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LIBRARY OF CONGRESS. 

%>P GopijnrAi 1?ii.- 

Shelf lU.23 



UNITED STATES OF AMERICA. 



THE DISEASES 



NERVOUS SYSTEM. 



DISEASES 



NERVOUS SYSTEM 



J. A. ORMEROD, M.D., OXON., F.R.C.P., LOND., 

Medical Registrar and Demonstrator of Morbid Anatomy at St. Bartholomew ■ 

Hospital ; Physician to the National Hospital for the Paralyzed and 

Epileptic, Queen Square, and to the City of ' Lotidon Hospital 

for Diseases of the Chest, Victoria Park. 




WITH NUMEROUS ILLUSTRATIONS. 



PHILADELPHIA: 

P. BLAKISTON, SON & CO, 

1012 Walnut Street. 
1802. 



^ 



Copyrighted, 1892, 

BY 

P. Blakiston, Son & Co. 



PRESS OF WM. F. FELL 4 C( 

1220-24 SANSOM STREET, 

PHILADELPHIA. 



PREFACE. 



The subject of nervous disease, attractive though it be, is 
apt to inspire the beginner with a feeling of dismay — it 
grows so fast, it has so many roots and branches, it presup- 
poses so much knowledge, and demands so much expenditure 
of time. Thoroughly to grapple with it, he will indeed 
require much patient clinical work, as well as study of those 
excellent and elaborate treatises which happily exist. This 
little volume is offered to him as no substitute for those, but 
only as an introduction to his work and outline map of terri- 
tory to be acquired; and should it thus prove to him, perhaps 
by its very smallness, an encouragement and aid, then it will 
have served its end. 



CONTENTS. 



CHAPTER I. 

ANATOMICAL AND PHYSIOLOGICAL INTRODUCTION. 

Nerve-cells, nerve- fibres, nerve-trunks — Spinal cord, its segments and 
tracts — Medulla oblongata, pons, arrd crura cerebri — Cerebellum — 
Cerebrum, its cortex, white matter, ganglia, and vessels, . . pp. 13-74 



CHAPTER II. 

MORBID ANATOMY OF NERVOUS SYSTEM. 

Disease of nervous parenchyma, inflammation, softening, abscess, degen- 
eration — Extrinsic disease, of vessels, bones, meninges : tumors, 

PP- 75-90 

CHAPTER III. 

ON CERTAIN GENERAL SYMPTOMS AND METHODS OF INVESTIGATION. 

Motor and sensory paralysis, and other anomalies of motor and sensory 
functions — Reflex actions — Inco-ordination — Vertigo — Speech defects 
— Coma, etc., pp. 91-121 

vii 



Vlll CONTENTS. 

CHAPTER IV. 

SYMPTOMS REFERABLE TO THE ORGANS OF SPECIAL SENSE. 

The eye : paralyses of ocular movements, affections of fundus oculi, affec- 
tions of vision — The sense of hearing — The senses of smell and taste, 

pp. 122-147 

CHAPTER V. 

SYMPTOMS REFERABLE TO SPECIAL DISTRICTS. 

Electrical examination — The face: paralysis, spasm, neuralgia, hemi- 
atrophy — The tongue, palate, larynx, respiration — The upper limb : its 
muscular mechanism, nerve-supply, and nerve-trunks — The trunk, 
neck; erect posture — The lower limb: its muscular mechanism and 
nerve-supply; walking; sciatica pp. 148-195 



CHAPTER VI. 

NEURITIS: ORGANIC SPINAL DISEASES. 

Neuritis, acute, peripheral ; diphtheritic palsy ; lead palsy — Spinal menin 
gitis; caries and cancer of vertebrae — Myelitis: infantile paralysis; 
degenerative diseases of cord ; muscular atrophies ; syphilis and 
tumors of the cord ; syringo-myelia, pp. 196-249 



CHAPTER VII. 

ORGANIC CEREBRAL DISEASE. 

General and localizing symptoms — Disease of dura mater ; thrombosis of 
sinuses — Meningitis: acute, tubercular, basal, epidemic — Cerebral 
disease : abscess, hemorrhage, softening, hemiplegia of long standing, 
hemiplegia in children, tumors, hydrocephalus, syphilis, . pp. 250-290 



CONTENTS. IX 

CHAPTER VIII. 

DISEASES OF WHICH THE ORGANIC BASIS IS NOT KNOWN. 

Epilepsy; chorea; tetany; paralysis agitans; writer's cramp; migraine; 
neuralgia; hysteria; trance; catalepsy; hypnotism; neurasthenia, 

pp. 291-326 



LIST OF ILLUSTRATIONS. 



FIG. PAGE 

1. Transverse sections of spinal cord, showing the shapes of the 

gray matter at different levels, 17 

2. Diagram to illustrate the chief connections of the anterior and 

posterior nerve-roots, 20 

3. Diagram of a reflex arc, 21 

4. Diagrammatic sections of spinal cord to show the tracts in the 

white matter, and grouping of the cells in the gray matter, . 24 

5. Transverse section through lower part of decussation of the 

pyramids, 30 

6. Transverse section through upper part of decussation of the 

pyramids, 31 

7. Transverse section of medulla, a little below the calamus scrip- 

torius, 31 

8. Ditto, at lower part of fourth ventricle, 33 

9. Diagrammatic sections through medulla, pons, and crura, ... 36 

10. Diagram to show nerve-nuclei in fourth ventricle, dorsal aspect 

(after Erb), 37 

11. Ditto, lateral aspect (after Erb), 38 

12. Base of brain (from Heath's Anatomy), 39 

xi 



XU LIST OF ILLUSTRATIONS. 

FIG. PAGE 

13. Transverse section of medulla, just below pons, 41 

14. Transverse section of pons through eminentia teres, 42 

15. Ditto, through origin of* fifth nerve (from preparation by Dr. 

Tooth), 43 

16. Ditto, at level of inferior corpora quadrigemina, 45 

17. Transverse section through crura, between superior and inferior 

corpora quadrigemina (from preparation by Dr. Tooth), . . 45 

18. Ditto, at level of superior corpora quadrigemina (from prepara- 

tion by Dr. Tooth), 46 

19. Superficial origins of cranial nerves (from Quain's " Anatomy "), 47 

20. Diagram to show connections of the cerebellum, 51 

21. Diagram of external surface of cerebral hemisphere, 54 

22. Ditto, upper surface, 55 

23. Ditto, mesial surface, 58 

24. Ditto, lower surface, 59 

25. Diagram of motor and sensory centres of cortex cerebri, external 

surface, 61 

26. Ditto, mesial surface, 62 

27. Horizontal section, diagrammatic, through cerebral hemispheres, 65 

28. Transverse vertical sections, diagrammatic, through cerebral 

hemispheres, 66-69 

29. Distribution of arteries on surface of cerebral hemispheres, ex- 

ternal aspect, 72 

30. Ditto, mesial aspect, 72 

31. Secondary degeneration of pyramidal tracts, 79 

32. Secondary ascending degeneration in postero-median columns, 80 

33. Secondary degeneration, ascending and descending, after trans- 

verse myelitis, 81 



LIST OF ILLUSTRATIONS. Xlll 






PAGE 



34. Diagram to show the general arrangement of the motor tract, 

and the effect of lesions at various points, 94 

35. Diagram to show axes of rotation produced by the ocular muscles 

(modified from Bristowe), 123 

36. Diagram to show the lines of movement produced by the ocular 

muscles (after Bristowe), 123 

37. Diagram to illustrate squint from paralysis of left external rectus, 125 

38. Diagram to illustrate the mechanism of conjugate lateral move- 

ments of the eyes, 129 

39. Healthy optic disc (from Nettleship, after Jager), 133 

40. Severe optic neuritis (from Nettleship, after Hughlings Jackson), 134 

41. Simple atrophy of disc (from Nettleship, after Wecker), ... 135 

42. Atrophy of disc from spinal disease (from Nettleship, after 

Wecker), 136 

43. Atrophy of disc after papillitis (Nettleship), 136 

44. Field of vision for white and colors (from Ross, after Gowers), 139 

45. Diagram to illustrate the distribution of fibres from the occipital 

lobes to the lateral halves of the retina, 141 

46. Diagram to illustrate the concentration of the current under the 

point of application of the smaller electrode, 152 

47. Diagram of the cutaneous nerve-supply of the face and head 

(after Flower), 161 

48. Complete paralysis of left vocal cord (after Ziemmsen), . . . 164 

49. Complete paralysis of both vocal cords (after Ziemmsen), ... 164 

50. Bilateral paralysis of posterior crico- arytenoids (after Ziemm- 

sen), 165 

51. Bilateral paralysis of internal thyro-arytaenoids (after Ziemm- 

sen) 165 



XIV LIST OF ILLUSTRATIONS. 

FIG. PAGE 

52. Paralysis of right serratus magnus (from Duchenne), .... 172 

53. Incomplete paralysis of the interossei (after Duchenne), . . . 174 

54. Paralysis and wasting of intrinsic muscles of hand (main en 

griffe) (after Duchenne), 175 

55. Atrophy of thenar muscles (after Duchenne), 175 

56. Diagram of cutaneous nerve-supply of upper limb (after 

Flower), 177, 178 

57. Diagram of cutaneous nerve-supply of lower limb (after 

Flower), 191, 192 

58. Tabes dorsalis (sections of cord in), 215 

59. Postero-lateral sclerosis (sections of cord in), 223 

60. Disseminated sclerosis (sections of cord in), 226 

61-66. Maps of motor points (after Erb and De Watteville), . .327-337 



NERVOUS DISEASES. 



CHAPTER I. 



ANATOMICAL AND PHYSIOLOGICAL 
INTRODUCTION. 

Nerve-cells. — In spite of the complicated functions per- 
formed by the nervous system, the histological elements of 
which it consists are comparatively simple. If we except 
certain complicated terminal organs, such as the retina, organ 
of Corti, etc., we shall find that the bulk of it is made up of 
cells and fibres. The nerve-cells or ganglion-cells vary in 
size and appearance ; some are small and rounded, others 
larger and bipolar, as in the "vesicular" columns of the 
cord ; others arrow-headed, as in the cortex cerebri ; others 
with several processes, as in the anterior gray columns of the 
cord. The large cells have a distinct nucleus and nucleolus, 
and often one of the processes is continuous with the "axis 
cylinder" of a nerve-fibre. Collections of such cells are 
found in the ganglia of the peripheral nervous system ; and 
cells united by a network of small fibres form the gray matter 
of the spinal cord, the cerebral ganglia, and the cerebral 
cortex. 

Nerve-fibres. — The essential part of a nerve-fibre is the 
central filament, called the "axis cylinder." There are, 
however, two varieties of nerve-fibres. In the one the axis 
cylinder is embedded in a layer of soft white material, akin 
to fat in its chemical reactions, which is called the myeline 
2 13 



14 NERVOUS DISEASES. 

or medullary sheath. Around this again is a fine envelop, 
bearing on its surface nuclei and called the nucleated sheath 
of Schwann. At certain intervals the medullary sheath is 
interrupted, and so the sheath of Schwann approaches the 
axis cylinder; these intervals are called the nodes of Ranvier. 
Such is the structure of a white or " medullated " nerve-fibre. 
The other variety is the non-medullated or gray fibre ; it con- 
sists simply of an axis cylinder and sheath of Schwann without 
any intervening myeline. The medullated nerve-fibre is par- 
ticularly associated with the cerebro-spinal system of nerves, 
the non-medullated with the sympathetic ; there is neverthe- 
less a kind of medullated fibre, distinguished principally by 
its very small calibre, which probably ranks with the sympa- 
thetic nerves. 

The function of nerve-fibres is simply to transmit nervous 
impulses; while cells not only transmit them, but combine, 
re-arrange, modify, and perhaps produce them. Again, there 
is this important difference as to the life of cells and fibres : 
nerve-fibres (at any rate peripheral nerve-fibres) when destroyed 
can be regenerated ; nerve-cells, so far as we know, cannot : 
and, further, the life of the fibre is in most cases dependent 
upon the cell with which it is connected, for if the connection 
be broken or the cell destroyed, then the fibre dies. 

Nerve-trunks. — The nervous elements are held together 
in the peripheral nervous system by envelops of connective 
tissue. Not only has each fibre its sheath of Schwann, but 
the bundles and nerve-trunks have additional connective- 
tissue sheaths, endo-, peri-, and epi-neurium, which protect 
and unite them, and convey to them their nutrient vessels. 
In the nerve centres, the white fibres lack the sheath of 
Schwann ; the nervous elements lie embedded in a substance 
called neuroglia, a granular-looking material containing an- 
gular cells (cells of Deiters). 

General Connection of Spinal and Sympathetic 
Systems. — The system of peripheral nerves consists of two 



INTRODUCTION. 1 5 

parts, the cerebro-spinal nerves and the sympathetic ; of 
which the former are distributed mainly to the skin and skele- 
tal muscles, the latter to the viscera and blood-vessels. The 
sympathetic is disposed on either side of the vertebral column 
in the form of a chain of ganglia, from which nerves run 
forward to form the large plexuses, cardiac, solar, pelvic, etc., 
which supply the adjacent viscera and blood-vessels. But it 
is closely connected with the cerebro-spinal system by the 
nerve-trunks called the "rami communicantes." This will 
be seen, if we proceed to consider the general arrangement of a 
cerebro-spinal nerve. Such arrangement is seen at its simplest 
in a nerve from the dorsal region. 

The nerve commences at its origin from the spinal cord in 
two roots, anterior and posterior. These are similar in struc- 
ture except for the fact that upon the posterior root is placed 
a ganglion. But their function is different : the anterior root 
is efferent, carrying impulses from the cord ; the posterior is 
afferent, carrying them to the cord. The roots join to form 
a mixed nerve, in which afferent and efferent fibres are united 
in a common envelop. This nerve divides into branches, 
a posterior and anterior, still of mixed function, and going to 
the skin and muscles of the back, and of the intercostal space 
respectively. Bui this is not all, for the " ramus communi- 
cans " opens a path by which fibres both come and go between 
the sympathetic and the spinal cord. Efferent fibres from the 
spinal cord pass out via the anterior root down the " ramus 
communicans" to the sympathetic ganglia. In this part of 
their course they are medullated fibres, though distinguished 
by being of a very fine calibre ; but after issuing from the 
sympathetic ganglion for distribution they are found to have 
lost their myeline sheath, and have become typical gray, sym- 
pathetic fibres. In a similar manner afferent fibres ascend 
from the sympathetic, to join the posterior spinal root, and 
thus enter the spinal cord. 

There are certain levels in the cord at which this connec- 



1 6 NERVOUS DISEASES. 

tion with the sympathetic is best marked. Thus, at the upper 
cervical region, a large outflow of fibres takes place from the 
cord to the sympathetic cervical ganglia, and thence to the 
cardiaG plexus ; and again in the upper thoracic region to the 
ganglia whence the splanchnic nerves arise. 

At other levels the sympathetic connection is less import- 
ant, and the spinal system reaches a higher and more complex 
development. This takes place at the cervical and lumbar 
enlargements, where the nerves for the limbs are given off. 
Here the roots are combined into the well-known plexuses, 
from which again the main nerve-trunks originate : by this 
means each nerve-trunk is brought into connection with more 
than one nerve-root, and more than one segment of the cord. 

Spinal Cord and Membranes. — The spinal cord reaches 
from the occipital foramen to the lower border of the first lum- 
bar vertebra. It is here continued by the leash of nerves 
known as the cauda equina. In the cauda equina are com- 
prised all the nerves from the second lumbar downward. 
Both these nerves, and also those immediately above them, 
have to run some way downward before they make their exit 
from the spinal canal. 

The envelops of the cord are, the dura mater, which forms 
a tube within, but quite detached from, the bony canal ; the 
arachnoid, which, by its denticulate processes, serves to sus- 
pend the cord within the dura ; and the pia mater, which 
invests the cord closely and sends into its substance septa 
which carry its nutrient vessels. 

Physiologically, the cord may be considered either as a 
centre (or rather a series of centres) for reflex actions, for the 
co-ordination and distribution of impulses proceeding from 
the brain, and for nutrition, particularly of the muscles — or 
else as a connecting path between the brain and the periphery. 
Similarly, in dealing with its anatomy, we may treat it either 
as a series of segments or as an aggregation of longitudinal 
tracts of fibres. 



INTRODUCTION. 



17 



Upper cervical region. 



Cervical enlargement ; 
Upper part. 



Middle part. 



Lowest part. 



Upper dorsal region. 




Lower part. 



Transverse Sections of Spinal Cord, showing the Shapes of the Gray 
Matter at Different Levels. 
The white matter has been stained black (according to Pal and Weigert's method), 
while the gray matter remains unstained. 



1 8 NERVOUS DISEASES. 

Spinal Segment. — The division of the cord into seg- 
ments is chiefly useful in considering the gray matter. Each 
segment corresponds in level to a pair of nerve-roots. It 
consists of two bilateral symmetrical halves ; in each of which 
there is an anterior and posterior "horn" of gray matter, 
corresponding to the anterior and posterior nerve-roots. The 
shapes of these horns differ in different segments, that of the 
anterior horn particularly, which is larger at the levels of the 
cervical and lumbar enlargements. Here also are best devel- 
oped its characteristic cells. 

The horns of each lateral half are united by a commissure of 
gray matter, in which is seen the central canal of the cord. 
Immediately in front of this gray commissure at the base of 
the anterior fissure is a commissure of white fibres. 

Anterior "Horns" and Anterior Cornual Cells. — 
The anterior horns, like the anterior nerve-roots, are motor in 
function, being concerned with efferent impulses. They 
contain, in addition to the fine plexus of nerve-fibres which 
pervades the gray matter, large nerve-cells, multipolar, but 
having one process which gives direct origin to a fibre of 
the anterior nerve-roots. From the cornu these fibres can 
be seen, passing forward in separate bundles through the 
white columns to the periphery. The cells are arranged 
in groups (Fig. 4, A and c), more or less well defined, and 
varying somewhat in different levels of the cord : («) along 
the inner margin of the horn (internal group) ; (/3) at its an- 
terior and antero-lateral margin (anterior and antero-lateral 
groups); (j) at its postero-external angle (postero-lateral or 
external group). In some parts of the cord there is (<J) a 
central group. 

As the cells form the starting-point for the fibres of the 
anterior nerve-roots, so they are the terminal point of the 
fibres which convey motor impulses from the brain (fibres of 
the pyramidal tract). Such impulses are probably grouped 
and re-arranged in the gray matter of the anterior horns. 



INTRODUCTION. 19 

They are connected also by the gray matter with the nerves 
that enter the cord by the posterior roots, forming thus part 
of the spinal centre for reflex action. In addition they 
maintain the nutrition of their efferent nerve-fibres and of 
the muscles in which these end. Destructive disease of the 
cells therefore causes paralysis of the muscles which they 
supply, loss of the reflex actions subserved by them, and, in 
addition, wasting of the muscles, usually accompanied by 
changes in their electrical reactions. Blueness and coldness 
of the limb (vaso-motor paralysis) usually occurs. Disease 
of the anterior nerve-roots produces practically the same 
effects. 

Posterior Horns and Cells. — The posterior gray horns 
contain, in most segments of the cord, but few and small cells. 
At certain levels, however, there are some important groups. 
One of these is known as the posterior vesicular column of 
Clarke, or, more briefly, as Clarke's column (Fig. 4, b). It 
extends from the third lumbar segment upward through the 
dorsal region. It consists of largish bipolar cells with axis 
cylinder processes ; these are set in the midst of tracts of fine 
white fibres. Its position (as seen in transverse section) is at 
the inner part of the posterior horn, near the junction of it 
with the gray commissure. By some authorities, these cells 
are regarded as the point of origin for the fibres of the cere- 
bellar tract ; by others, as the cells which preside over the 
fine medullated efferent nerves to the sympathetic, viscera, 
and vessels, just as the anterior cornual cells preside over the 
motor nerves and skeletal muscles. 

Another column of cells is known as the " intermedio- 
lateral tract." It is situated at the outer side of the gray 
matter at the junction of the anterior and posterior horn. It 
is most distinct in the dorsal region, in the upper dorsal and 
lower cervical region forming a lateral "process" which 
projects outward from the gray matter. 



20 NERVOUS DISEASES. 

Posterior Nerve-roots. — The posterior nerve-roots enter 
the cord in one large bundle ; but this splits into two divisions. 
One of these, the lateral or external division, goes for the 
most part directly into the posterior horn, through the 
"substantia gelatinosa " (i.e., a tract of gray granular 
material which forms a cap, as it were, to the posterior 
horn) ; but a small number of fine fibres turn upward and 
run longitudinally in the cord at the tip of the posterior gray 
horns, forming here Lissauer's tract. 

Fig. 2. 

Anterior nerve-root. 



Anterior root-fibres originating in anterior 
horns. 



Gangl 




j Cell groups of anterior horns. 
Posterior nerve-root. 



Fine fibres going to Lissauer's tract. 
Fibres entering posterior horn directly. 

Fibres which arch through postero-external 

column and then enter posterior horn. 
Fibres which join postero-median column. 



Diagram to Illustrate the Chief Connections of the Anterior and 
Posterior Nerve-roots. 



The second division (median or internal) curves inward 
into the postero-lateral column, and, after running upward 
therein for a short way, partly curves outward again into the 
base of the posterior horn, partly runs inward to join the 
postero-median column. 

The posterior nerve-roots convey to the nervous centres 
all afferent impulses from the various organs of the body, 
whether these be such as, ascending to the cortex cerebri, give 
rise to actual sensation, or such as call into action lower cere- 



INTRODUCTION. 



21 



bral centres, or such as, entering the gray matter of the cord, 
give rise to the simpler spinal reflexes. Of the course pursued 
by sensory impulses after they reach the cord we know, ana- 
tomically, nothing ; but it would appear from physiological 
experiment and some facts of disease, that soon after entering 
the cord they cross to the other side.* The course of sundry 
upward nerve -tracts to the cerebellum and elsewhere we 
know, but we do not know their function. 



Afferent path to 
cerebrum. 




JBgT IV I 



Efferent path from 
cerebrum. 



Diagram of a Reflex Arc. 
(The numbers correspond to those in the text). 



Reflex Arc. — The path for reflex action within the cord 
is provided by the gray matter which joins the posterior 
nerve- roots to the anterior cornua. Thus, so far as a single 
spinal segment is concerned, the " reflex arc," as it has been 
termed, consists of the following parts: — 

(i) Peripheral (sensory) organ. 

(2) Afferent nerve (fibrils of origin and nerve-trunk). 



* This statement, in the light of recent researches, may need revision. 



22 NERVOUS DISEASES. 

(3) Posterior nerve-root (extra and intra-spinal), 

(4) Fibres of gray matter. 

(5) Anterior cornual cells. 

(6) Anterior nerve-roots (intra and extra-spinal). 

(7) Efferent nerve (nerve-trunk and terminal fibres). 

(8) Terminal (motor) organ. 

Destruction of any of these parts will annul the reflex ; but 
where 5, 6, 7 or 8 is destroyed, there will be motor paralysis 
as well. 

The more detailed consideration of the various spinal 
reflexes we shall defer for the present. 

Motor and Sensory Functions of Different Seg- 
ments. — The motor and sensory functions of the various 
spinal segments have yet to be considered — /. <?., what 
muscles are supplied by the anterior cornual cells and 
anterior nerve-roots of each segment, and what areas ot 
skin by its posterior roots. In the dorsal region of the 
cord this is comparatively simple, since the distribution 
of each nerve-root is simple and can be ascertained 
anatomically. At the levels of the large limb-plexuses mat- 
ters are more complicated, and the functions of each spinal 
segment are less completely known. The present data for 
our knowledge consist of (a) experiments upon the several 
nerve-roots — viz.: division of them, with subsequent stimula- 
tion of the peripheral end ; (/9) dissection of nerve-bundles 
downward, from the roots through the plexuses and nerve- 
trunks to their ultimate distribution; (y) observation of the 
effects resulting from limited or gradually progressive cord 
lesions, the locality of the lesion being determined post-mor- 
tem. It is usually assumed that the function of each nerve- 
root corresponds to that of its spinal segment; and there is a 
certain agreement (though not altogether complete) between 
the result of the three methods we have mentioned. 



INTRODUCTION. 



23 



The following tables (taken from Thorburn*) are based on 
the third or clinical method : — 



Cervical Enlarge- 
ment. 


Motor Distribution. 


4th cervical segment 


( Supra- and infra-spinatus ) 
■I Teres minor ? j 


supplies 








(_ Biceps 






( Brachialis anticus 


5 th do 


do. 


■i Deltoid 

^Supinator longus brevis 
f Subscapularis 

Pronators 
| Teres major 


6th do. 


do. 


•j Latissimus dorsi 

Pectoralis major 

Triceps \ 
^Serratus magnus J 






7th do. 


do. 


Extensors of wrist 


8th do. 


do. 


Flexors 


1st dorsal 




Intrinsic muscles of hand 


1st lumbar 




None 


2d do. 




None 
("Sartorius 


3d do. 




-C Adductors of thigh 
(Flexors of thigh 
J Extensors of knee 
\ Abductors of thigh 


4th do. 





5th do. 
1st sacral 



Hamstring muscles 

! Calf-muscles 
Glutei 
Peronei 
Extensors of ankle f 
Intrinsic muscles of foot 



Sensory Distribution. 

Skin over deltoid and outer 
aspect of arm and forearm. 



Central parts of arm and fore- 
arm on anterior and pos- 
terior aspects. 



f Little finger and inner side 
\ of hand, forearm and arm. 
Ilio-hypogastric and ilio- 
inguinal. 
Outer and (?) upper part of 
thigh. 
'Anterior aspect of thigh 
j below 2d lumbar. 

Anterior and inner part of 
leg. 

Back of thigh, except in 
distribution of 1st, 2d 
and 3d sacral. 
£ A narrow strip on back 
g ! of thigh, back of leg, 
.w> f and ankle ; sole ; part 
v of dorsum of foot. 



3d sacral 



] Perineal muscles, viz., 
I erector penis, transver- 
salis perinei, accelera- 
tor urina, etc. 
Bladder and rectum. 



Perineum, external geni- 
tals, "saddle-shaped" 
area on back of thigh. 



Longitudinal Conducting Paths or " Tracts " in 
the Cord." — Viewed as a conducting path to and from the 
brain, the spinal cord may be mapped out into various longi- 
tudinal paths or " tracts." These are formed from the white 
matter of the cord. Most of them are not distinguishable 



* " Surgery of Spinal Cord," pp. 4, 42, 1 1 1 . 
f i.e., dorsi flexors. 



24 



NERVOUS DISEASES. 



Fig. 4. 
Diagrammatic sections of spinal cord in — 

(a) Cervical, 

(b) Upper dorsal, 

(c) Lumbar regions : to show the tracts in the white matter (left 
half), and the grouping of the cells in the gray matter (right half). 




Direct pyramidal 

tract. 
Ground fibres. 

Anterolateral tract 

Lateral limiting 

layer. 
Cerebellar tract. 

Crossed pyramidal 
tract. 
Lissauer's tract. 

Postero-lateral column. Postero-median column. 
A. In Cervical Region. 
Direct pyramidal tract 
Ground fibres. . 



Postero-lateral 
cell-groups of 
anterior horns. 



Antero-lateral tract. 

Lateral limiting layer. 
Cerebellar tract. 

Crossed pyramidal 
tract. 

Lissauer's tract. 
Postero-lateral column. 




Intermedio-lateral pro- 
cess and cells. 

Posterior vesicular col- 
umns (columns of 
Clarke). 



Postero-median column. 
B. In Dorsal Region. 



Ground fibres. 

Antero-lateral tract? 

Lateral limiting layer 

Crossed pyramidal 
tract. 

Lissauer's tract. 

Postero-lateral col- 
umn. 




Anterior. 

Antero-lateral. 

Postero-lateral cell- 
groups of anterior 
horns. 

Posterior vesicular 
columns (lower ex- 
tremity of). 



Postero-median column. 
C. In Lumbar Region. 



INTRODUCTION. 2$ 

in the healthy cord of an adult, anatomically, but their exist- 
ence is determined partly by the definite courses taken by 
degenerative processes, primary or secondary, in the cord ; 
partly by the differences in the date of their development, 
the date, that is, at which the nerve-fibres of the various tracts 
become clothed with myeline. Some certainly, and probably 
all, of these tracts have distinct functions. 

Motor or "Pyramidal" Tract. — The motor tract is 
the best known, and we will begin with this. Taking a 
transverse section, say at the cervical enlargement, there are 
present in the antero-lateral columns {i.e., the parts between 
the anterior fissure and the posterior horns) — 

(a) The crossed, or lateral, pyramidal tract. 

(/?) The direct, or anterior, pyramidal tract. 

These two are the continuation downward of the anterior 
pyramid of the medulla (whence the name pyramidal), and 
thereby of the fibres which carry motor impulses from the 
brain. 

The crossed, or lateral pyramidal tract represents that 
(larger) portion of the motor fibres which have decussated at 
the lower part of the medulla ; the direct or anterior pyramidal 
tract, sometimes also called the column of Tiirck, is the 
(smaller) non-decussated portion. 

The direct pyramidal tract is seen in transverse section as 
a narrow strip along the edge of the anterior fissure. Traced 
down the cord, it usually ends about the middle dorsal region, 
but it has been found to reach as low as the lumbar cord. 
How its fibres terminate is uncertain : probably they cross 
(? by the anterior white commissure) and so reach the anterior 
horns of the opposite side. 

The crossed pyramidal tract appears in the posterior part 
of the lateral columns, as an area roughly triangular, with its 
base toward the periphery and its apex running up into the 
angle between the anterior and posterior horns. Posteriorly 
it abuts upon the posterior horn, but for the most part it does 



26 NERVOUS DISEASES. 

not reach quite so far as the gray matter; a thin zone of 
white matter, called the lateral limiting layer, separates it 
therefrom. Neither does it, at least in the cervical* and 
dorsal regions, quite reach the surface of the cord, since the 
cerebellar tract, presently to be mentioned, here occupies the 
periphery. But in the lower dorsal and lumbar regions, 
where the cerebellar tract does not exist, the crossed pyramidal 
tract extends to the surface. This tract reaches, longitudi- 
nally, down to the upper sacral region. It becomes smaller 
as it passes downward, because fibres are continually leaving 
it to terminate in the anterior cornual cells. The actual 
path of the fibres has not been determined ; but it is certain, 
since this tract constitutes the main motor path from the 
brain, that its fibres must eventually be connected with 
these cells. 

Cerebellar Tract. — The direct cerebellar tract occupies, 
in transverse section, a narrow zone at the periphery of the 
lateral columns of the cord, exterior to the crossed pyramidal 
tract. At most levels this zone extends from the tip of the 
posterior horn forward as far as a line drawn horizontally 
through the central canal. In the lower dorsal region where 
the tract is small, and also about the third cervical segment 
where it is shifted a little forward, it does not extend quite 
so far backward as the posterior horns. The tract contains 
afferent fibres passing to the cerebellum. They originate, 
according to some authorities, in the cells of the posterior 
vesicular column of Clarke. 

The tract begins to be visible in the lower dorsal regions 
and passes upward, in the position described above, to the 
medulla. It then enters the restiform body, and ends in the 
middle lobe of the cerebellum. 



* Except in the upper cervical region, where, owing to a forward move- 
ment of the cerebellar tract, the posterior part of the crossed pyramidal tract 
comes to the surface of the cord. 



INTRODUCTION. 2J 

Antero-lateral Ascending Tract. — The "antero- 
lateral ascending tract " constitutes another tract of ascending 
fibres. In transverse section, it occupies the periphery of the 
cord in front of the cerebellar tract, reaching forward nearly 
to the margin of the anterior fissure. But it also dips into 
the cord, sending a process inward in front of the crossed 
pyramidal tract toward the gray matter, and filling up any 
place left between the cerebellar and the crossed pyramidal 
tract. Its fibres are believed to originate in the gray matter 
through the whole length of the cord, commencing at any 
rate at a lower level than those of the cerebellar tract. Pos- 
sibly it bears some definite relation to the posterior nerve- 
roots. When traced upward into the medulla it maintains, 
according to Tooth, a position at the periphery, just posterior 
to the olivary body. It thus becomes separated from the 
cerebellar tract, which here passes backward toward the resti- 
form body. It is by some authors thought to end in the 
lateral nucleus of the medulla. Others maintain that it is 
really part of the cerebellar tract, and ascends like it via the 
restiform body to the cerebellum. 

The remainder of the antero-lateral columns of the cord — 
viz., all that part of the white matter, from the anterior fissure 
backward to the posterior gray horn — which has not been 
included in the various tracts we have described, constitutes 
what has been called the anterior and lateral " ground fibres," 
and the " mixed lateral zone." We shall not here enter into 
a description of these parts. 

Structure of Posterior Columns. — Each posterior 
column is divisible into a postero-lateral and a postero-median 
portion. A rough anatomical distinction between the two is 
afforded by a septum which passes inward from the pia mater. 
The postero-lateral column, called also the cuneate fasciculus 
or the column of Burdach, constitutes the external division. 

Postero-lateral Column or Column of Burdach. — 
This is the stripe of white matter which lies next to the pos- 



28 NERVOUS DISEASES. 

terior gray horn, its extent varying at different levels in the 
cord. It has a close relation to the posterior nerve-roots ; 
some of these traverse the column horizontally, passing 
through it into the neck of the posterior gray horn ; while 
others, after entering the column, run upward in it a little 
way, and then join — some the gray matter, some the postero- 
median column. Their place in the postero-lateral column 
is taken by a fresh supply from other nerve-roots. The fibres 
are afferent and degenerate upward. But owing to the 
arrangement just stated — viz., the continuous replacement of 
fibres from the nerve-roots — it is found that these columns do 
not (in the case of a transverse lesion) degenerate for any 
great distance from the original lesion. That part of the 
column which is traversed by the fibres entering from the 
posterior roots — viz., the part adjacent to the gray horn as it 
nears the periphery — is of importance, because disease here 
cuts the posterior root-fibres and causes disappearance of 
tendon reflex.* The postero-lateral columns are continued 
into the lower part of the medulla, where they terminate in 
the post-pyramidal nuclei. 

Postero-median, or Column of Goll. — The postero- 
median columns, otherwise called the columns of Goll, are 
placed on each side of the posterior fissure ; the two tracts 
together form, in the lower parts of the cord, a triangle with 
the base at the periphery, in the upper parts a narrow strip 
bordering the fissure on .each side. These tracts are to a 
great extent formed from fibres which come from the posterior 
nerve-roots and have run a short course (as described above) 

* Westphal defines the area in the lower dorsal and upper lumbar regions 
thus: It forms a rough triangle whose anterior side is the posterior edge of 
the gray matter, its posterior the periphery of the cord, its inner side a line 
drawn backward from the re-entrant angle formed by the gray matter of 
the posterior horn, and parallel with the posterior fissure. This he calls 
the zone of entry of the posterior nerve-roots {\Vurzel-eintrilt-zone), and 
disease here causes loss of patellar tendon reflex {vide Fig. 59). 



INTRODUCTION. 29 

in the postero-lateral column. After entering the postero- 
median column, the fibres run in it upward without interrup- 
tion to the medulla (fasciculus gracilis) where they terminate 
in the postero-median nucleus. The fibres that enter from the 
lower nerve-roots place themselves, as they ascend the cord, 
behind those that enter from the upper nerve-roots. There- 
fore, in a lesion of the lower part of the cord, degeneration, 
although traceable through the whole length of the columns, 
is limited in the cervical region to their posterior part. 

The two postero-median columns do not decussate ; the 
posterior nerve-roots of each side are continued upward in the 
column of the same side. 

The postero-median, like the postero-lateral columns, are 
composed of afferent fibres. Yet neither of them, so far as 
we know, in spite of their intimate connection with the pos- 
terior nerve-roots, forms the path for common cutaneous 
sensation. 

To the account of these, the principal known tracts, we 
may add a few minor points. 

1. Between the postero-median and postero-lateral tracts, 
both of which are, as we have said, afferent or ascending, is a 
small tract of fibres, which, in a transverse lesion of the cord, 
degenerates downward for a short distance. This is called, 
from its shape, the comma-shaped degeneration. 

2. Low in the lumbar region, on either side of the posterior 
fissures, and enclosed between the two postero-median tracts, 
is a small area, shaped like a bi-convex lens, which is some- 
times found intact, while the postero-median tracts are de- 
generated. 

3. A small ascending tract has been described at the tip of 
each posterior cornu between this and the periphery of the 
cord. It is reckoned by some authors into the posterior, by 
others into the lateral, columns. It runs the whole length of 
the cord and conducts and degenerates upward. It consists 
of fine medullated fibres derived from the posterior roots 

3 



3<D NERVOUS DISEASES. 

(? coming from the sympathetic), and probably terminates at 
various levels in the posterior gray horns. It is called 
Lissauer's tract, and it is said to degenerate early in cases of 
locomotor ataxy. 

4. A few fibres in the antero-lateral columns of the cord 
are found to degenerate in a downward direction. 

Medulla Oblongata. — Numerous alterations take place 
in the cord during its passage upward into the medulla. 
The most striking of these alterations are — 

I. The decussation of the pyramids. 

II. The development of sundry gray nuclei, some of which 
are not represented in the cord. 

III. The opening out of the central canal to form, on the 
dorsal aspect of the medulla, the fourth ventricle. 

Fig. 5. 

Decussating pyramid. 

Anterior horn. 

/ ._.'■* J5' '-'13 Central gray matter. 

~ry Substantia gelatinosa Rolandi. 

Transverse Section through Lower Part of Decussation of the Pyramids 
(just above first cervical nerve). 

I. The motor fibres in each lateral column (crossed pyra- 
midal tract) as we trace them upward to the medulla, advance 
to the front, and cross each to the opposite side of the middle 
line (decussation of the pyramids), and there combine with 
the motor fibres of the opposite anterior columns (direct 
pyramidal tract) so as to form the anterior pyramids of the 
medulla. In thus crossing they cut off and throw to the sides 
a part of the anterior gray cornua. 

II. Nuclei of gray matter are developed in the following 
parts : — 

1. In the posterior columns of each side appear — 
a. The nucleus of the posterior median column, wherein 
the fibres of the posterior median column terminate. 




INTRODUCTION. 



31 



/?. The nucleus of the posterior lateral column, wherein the 
fibres of this column terminate. 

[These nuclei are sometimes called the post-pyramidal nuclei : 
besides receiving the fibres of the posterior column they 
give origin to fibres which pass brainward. These are called 



Fig. 6. 
Decussating pyramid. 
Anterior horn. 
Cerebellar tract. 
Substantia gelatinosa Rolandi. 
Nucleus of postero-lateral column. 
Nucleus of postero-median column. 
- Gray matter round central canal. 
Transverse Section through Upper Part of Decussation op Pyramids. 

arcuate fibres, from their peculiar curved course. They sweep 
forward through the deeper parts of the medulla beneath the 
gray matter which surrounds its central canal, and thus reach- 
ing its ventral aspect they decussate with each other, at a 
higher level than the decussation of the anterior pyramids. 




Fig. 7. 



Accessory olive. 

Lateral nucleus. 

Nucleus ambiguus. 



Arcuate fibres and formatio 
reticularis. 




Central canal and gray matter round it 
(hypoglossal and spinal accessory nuclei). 



Pyramidal tract. 

Olivary body. 
Inter-olivary layer. 
Substantia gelatinosa. 
Ascending root of fifth. 

Nucleus of postero-lateral 

column. 
Nucleus of postero-median 

column. 



Transverse S 



of Medulla, a little Below the Calamus Scriptorius. 



This is sometimes called the "superior pyramidal decussa- 
tion." A large proportion of them then passes brainward 
on either side of the middle line, between the olivary bodies, 
forming the " inter olivary layer," and eventually the " fillet." 
Others continue a curved course round the periphery of the 



32 NERVOUS DISEASES. 

medulla on its ventral aspect, encircling the anterior pyramid 
and the olivary body, and eventually join the restiform body.] 

2. Between the posterior and lateral column — the gray 
matter at the tip of the posterior cornu (caput cornu poste- 
rioris) enlarges to form the substantia gelatinosa of Rolando. 
This corresponds to a swelling on the surface of the medulla, 
which constitutes, as it were, an extra pyramid, known as the 
funiculus or tubercle of Rolando. 

[From the neighborhood of the tubercle of Rolando rises 
a nerve bundle, which passes brainward through the medulla 
up to the origin of the fifth nerve; this is the ascending root 
of the fifth nerve.] 

3. In the central and lateral parts of. the medulla — 

a. That part of the anterior gray cornu which has been cut 
off and pushed to the side by the decussation of the pyramids, 
partly remains in the form of distinct nuclei (motor nucleus 
of the vagus or nucleus ambiguus and antero-lateral nucleus), 
partly becomes mixed with white fibres derived from the an- 
terior and lateral columns of the cord, and thus forms a 
network of gray and white matter known as the reticular 
formation of the medulla. This reticular formation is con- 
tinued upward through the whole length of the medulla and 
pons, forming a sort of basis for the floor of the fourth ven- 
tricle, which it separates from the white strands which lie in 
the ventral parts of the medulla and pons. 

ft. The gray matter round the central canal, reinforced by 
that part of the anterior cornu which has not been decapi- 
tated, forms the nuclei of the hypoglossal and spinal accessory 
nerves. 

4. At a higher level (viz., as the fourth ventricle begins to 
open out) there appear on each of the anterior pyramids the 
large wavy capsules of gray matter known as the olivary 
bodies. These cause a well-defined egg-shaped prominence 
on the outside of the medulla. 

III. The central canal of the cord opens out posteriorly, 



INTRODUCTION. 33 

and forms the fourth ventricle. In the floor of this ventricle 
are found numerous important nuclei which we shall mention 
presently : on either side of it (at the level, that is, of the 
medulla) is the inferior cerebellar peduncle, or restiform body, 
containing the direct cerebellar tract, the fibres which connect 
the olivary body and cerebellum, and other fibres of connec- 
tion between the cerebellum and medulla and cord. 

Thus, when the level of the fourth ventricle has been 
reached, the arrangement of the constituents of the spinal 
cord has undergone a tolerably complete modification. 



Inter-olivary layer. 



Accessory nucleus of 
vagus. 

Root of vagus nerve. 

Ascending root of 
fifth. 
Respiratory bundle ' 

(ascending root / \ Upper end of post- 

ofglosso-pharyn- Hypoglossal Nucleus of vagus. pyramidal nuclei. 

S e£ ")- nucleus. 

'ransverse Section of Medulla at Lower Part of Fourth Ventricle. 



Region of Pons. — The parts of the nervous axis above 
this level — viz., the upper part of the medulla, the pons, and 
the crura cerebri — are very complicated. Yet a few general 
remarks may be applied to this region also. 

i. Like the cord, it consists of two symmetrical lateral 
halves : these (in the pons and medulla) are divided from each 
other by a median "raphe," a structure which conveys many 
fibres in a longitudinal direction, and receives and gives off 
others laterally. 

2. It is also divisible into a posterior (dorsal) and an ante- 
rior (ventral) part. In the latter run the motor tracts, form- 
ing distinct columns in the medulla (anterior pyramids) and 
in the crura cerebri, but split up into small isolated bundles in 




34 NERVOUS DISEASES. 

the pons, by the interlacement with them of the cross fibres of 
the pons or middle cerebellar peduncles. The posterior or 
dorsal division consists largely in the medulla and pons of the 
reticular formation, and of the nuclei of various cranial 
nerves, while between this and the ventral division runs the 
flat layer of longitudinal fibres known as the "fillet."* In 
the region of the crura cerebri the dorsal division of the ner- 
vous axis (called the tegmentum) is distinctly separated from 
the ventral division (called the crusta or pes pedunculi), by a 
layer of darkly pigmented cells called the substantia nigra. 
But these arrangements are complicated by — 
3. The strands of fibres which form the connections of the 
cerebellum. These form three sets of pillars or crura (a) 
below the pons, the inferior cerebellar peduncles or restiform 
bodies which, diverging from the medulla upon either side of 
the fourth ventricle, convey fibres from the cord and medulla 
below up to the cerebellum (,5) at the level of the pons, the 
middle cerebellar peduncles, which constitute the majority of 
the transverse fibres of the pons, and serve partly to connect 
the two lateral lobes of the cerebellum, partly to connect 
each lateral lobe with the opposite crus cerebri (as will be 
subsequently described) ; (f) above the pons, the superior 
cerebellar peduncles, which converge from the lateral lobes of 
the cerebellum, upward and toward the middle line of the 
tegmental division of the crura cerebri. 

* The fillet originates below in the inter-olivary layer (as above described) 
principally in connection with fibres from the post-pyramidal nuclei, passes 
upward between the ventral and dorsal divisions of the pons, and at the 
level of the crura cerebri divides; part of it (mesial fillet) retains for a 
time its former position— viz., between the crusta and tegmentum— 
and then ascends to the superior corpus quadrigeminum and optic 
thalamus (whence it is also called the superior fillet); part of it passes 
outward to the superficial part of the crus, round which it winds to reach 
the inferior corpus quadrigeminum (hence called the inferior or lateral fil- 
let) ; part of it, the most mesial part of all, turns in a ventral direction to join 
the crusta. 



INTRODUCTION. 35 

4. By the nuclei and root-fibres of the various cranial 
nerves. These will be described in detail presently. Roughly 
speaking, the nuclei form longitudinal columns of cells, 
which are disposed around the upper end of the spinal canal, 
around that continuation of it in the region of the crura 
cerebri which is called the Sylvian aqueduct, and between 
these levels, either in the floor of the fourth ventricle or some- 
what deeper in the formatio reticularis. Some of the motor 
nuclei (e. g., the hypoglossal and sixth) lie close to the middle 
line in the floor of the ventricle, having on their outer side in 
the more lateral parts of the ventricle sensory nuclei {e.g., the 
pneumogastric, glossopharyngeal, and auditory). Another 
set of motor nuclei — viz., the pneumogastric, glosso-pharyn- 
geal, facial, trigeminal — lie, as we have said, more deeply in 
the medulla, and farther from the middle line. This latter 
set represents that part of the anterior gray horn which has 
been cut off and thrust aside by the decussation of the pyra- 
mids, whereas the former set represents that part which has 
not been thus decapitated, while the sensory nuclei external 
to them represent the posterior spinal cornua thrown forward 
and outward by the opening out of the ventricle. The fibres 
from the nuclei mostly pierce the pons and medulla, and 
emerge either at its front or sides, excepting the fourth nerve, 
which emerges at the back and runs round to the front outside 
the central nervous axis, and one root of the auditory nerve 
which similarly runs round the restiform body. 

5. By certain comparatively small longitudinal nerve- 
bundles — viz., the ascending and descending roots of the fifth 
nerve — which connect this nerve with the parts above and 
below it ; the posterior longitudinal bundle, and the posterior 
respiratory bundle, which probably have some similar relation 
to the oculo-motor and glosso-pharyngeal nerves respectively. 

The general features of the medulla and pons may be seen 
in the diagrams (Fig. 9). They are as follows: — 

1. In a transverse section through the medulla — anterior or 



36 



NERVOUS DISEASES. 



ventral part consists of anterior pyramids (motor tract), 
olivary bodies, inter-olivary layer — posterior or dorsal part 

Fig. 9. 
Diagrammatic Sections through Medulla, Pons, and Crura. 

Olivary body. 

— Inter-olivary layer. 

Reticular formation. 

Deeply seated nerve-nucleus. 
Restiform body. 



Nerve-nuclei in floor of 
4th ventricle. 
A. Through Medulla at Lower Part of 4TH Ventricle. 

Pyramidal tract in (separate 
bundles) 





Reticular formation. 



Nerve-nucleus (stb)in floor of 
4th ventricle. 

Through Pons at Level of 5TH Nerve. 
Fronto-cerebellar tract. Geniculate fibres. 

Pyramidal tract. 

:^- '/ 7\. , Fibres to caudate nu- 
cleus. 
Temporo-occipital 



Substantia nigra. 
Red nucleus. 

Sylvian aqueduct. 




Gray matter round 
aqueduct (nucleus of 
3d nerve). 



Corpus quadrigeminum superius. 
C. Through Crura Cerebri at Level of Superior Corpora Quadrigem^ 



consists of reticular formation, nerve-nuclei (here hypoglossal 
and pneumogastric), restiform bodies. 



INTRODUCTION. 



37 



2. Through the pons — anterior or ventral part consists of 
transverse fibres of pons interlaced with the scattered longi- 
tudinal fibres of the pyramidal tracts — posterior or dorsal part 
consists of reticular formation, nerve nuclei, 5th, 6th, facial 
or auditory, according to level of section. Between the ante- 
rior and posterior parts are the longitudinal fibres of the 
fillet. 

3. Through the crura — anterior (ventral) and posterior 



Corpora quadrige- 
mina. 



Eminentia teres 

Striae acoustics 

Ala cinerea, 



Calamus scripto- 




Nucleus of in. 
Nucleus of iv. 

Motor nucleus of v. 

Sensory nucleus of v. 

Nucleus of vi. 

Nucleus of facial. 

Principal nucleus of 
auditory. 

Nucleus of glosso- 
pharyngeal. 

Nucleus of vagus. 

Nucleus of spinal ac- 
cessory. 

Nucleus of hypoglos- 
sal. 



Diagram of 4th Ventricle and Adjacent Parts, as seen from Dorsal As- 
pect, to show Positions of Nerve-nuclei. 
These are marked on the right-hand half. {After Erb.) 



(dorsal) divisions are well marked, being divided by the 
"substantia nigra." The tracts of nerve-fibres will be de- 
scribed later. The nerve-nuclei are those of the 3d and 4th. 
The central canal has again closed up and formed the Sylvian 
aqueduct. 

Nuclei of Cranial Nerves. — The origins of the cranial 
nerves must now be described in detail. Their general position 
may be studied in Figs. 10 and 11. 

The nucleus of the hypoglossal (Figs. 7, 8, 10, 11) reaches 
4 



38 



NERVOUS DISEASES. 



from the level of the striae acousticae downward to the top of 
the pyramidal decussation. In its lower part it lies in front 
of the central canal ; in the floor of the 4th ventricle it lies 
next to the middle line. The nerve-fibres run outward and 
forward, and appear on the surface between the olive and 
anterior pyramid. The nerve-trunk leaves the skull by the 
anterior condyloid foramen, and is distributed to the muscles 
attached to the hyoid bone, particularly to those of the 
tongue. 

Fig. 11. 



Root fibres of v. 



Superior olive. 



Root-fibres of facial. 

Root-fibres of vi. 

Olivary body. 

Pyramidal tract. 




Motor nucleus of v. 

Sensory nucleus of v. 

Nucleus of vi. 

Genu of facial. 

Nucleus of facial. 

Striae acousticse. 

Nucleus of auditory. 

Nucleus of glosso- 
pharyngeal. 

Nucleus of vagus. 

Nucleus of spinal ac- 
cessory. 

Nucleus of hypoglos- 



DlAGRAM TO SHOW POSITIONS OF PRINCIPAL NekVE-NUCLEI IN PONS AND 

Medulla, Side View. 
The organ is supposed to be split down the middle line, and the right half viewed from 
the mesial side. The most mesially situated nuclei are shaded, the others stippled. 
(After Erb.) 



The main nucleus of the spinal accessory, pneumogastric, 
and glossopharyngeal nerves (Figs. 7, 8, 10, 11, 13), may be 
reckoned as a continuous column which has nearly the same 
extent from above downward as the hypoglossal. The lowest 
part (nucleus of the spinal accessory) lies close to, and a little 
behind, the central spinal canal at its upper end ; the middle 
part (nucleus of the pneumogastric) lies underneath the ala 
cinerea near the apex of the fourth ventricle, that is to say, 
just outside the hypoglossal nucleus ; the upper part (nucleus 



INTRODUCTION. 



39 



of the glosso-pharyngeal) has a similar position higher up in 
the medulla, being in juxtaposition to the auditory nucleus, 




Base of Brain {from 

i. Longitudinal fissure. 

2. 2. Anterior lobes of cerebrum. 

3. Olfactory peduncle and bulb. 

4. Lamina cinerea. 

5. Fissure of Sylvius. 

6. Locus perforatus anticus. 

7. Optic commissure. 

8. Tuber cinereum and infundibulum. 

9. Third nerve. 

10. Corpus albicans. 

11. Fourth nerve. 

12. Locus perforatus posticus. 

13. Fifth nerve. 

14. Crus cerebri. 

15. Sixth nerve. 

16. Pons Varolii. 

17. Portio dura of 7th. 



Heath' s "-Anatomy "). 

18. Middle lobe of cerebrum. 

19. Portio mollis of 7th. 

20. Anterior pyramid. 

21. Glosso-pharyngeal nerve. 
22 Olivary body. 

23. Pneumogastric nerve. 

24. Lateral tract. 

25. Spinal-accessory nerve. 

26. Digastric lobe. 

27. Hypoglossal nerve. 

28. Cerebellum. 

29. Amygdala. 

30. Slender lobe. 

31. Posterior lobe of cerebrum. 

32. Posterior inferior lobe. 

33. Inferior vermiform process. 



which is outside and above it. The fibres of all these three 
nerves run forward and outward through the lateral parts of 



40 NERVOUS DISEASES. 

the medulla (piercing en route the ascending root of the fifth), 
and appear superficially behind the olivary bodies. They 
leave the skull by the jugular foramen. 

[The spinal part of the spinal accessory nerve is in reality a 
distinct nerve ; its fibres come from the cervical cord up 
through the foramen magnum into the skull ; it also leaves 
the skull by the foramen jugulare, and is eventually distributed 
to the trapezius and sterno-mastoid.] 

But, in connection with the origin of the three nerves in 
question, two additional structures must be considered. 
First, a column of cells (sometimes called the nucleus 
ambiguus) lying deep in the medulla in front of, and external 
to, part of the vagal nucleus : these cells (which may be con- 
sidered, as we have said, as part of the anterior cornu of the 
spinal gray matter, cut off and pushed sideward by the decus- 
sation of the pyramids) constitute the motor nucleus of the 
vagus and glosso-pharyngeal, the main nucleus being sensory. 
Secondly, a small round bundle of longitudinal nerve-fibres 
placed just outside the main glosso-pharyngeal and pneumo- 
gastric nuclei, not far from the surface of the fourth ventricle. 
It is continuous below with the lateral column of the cord. 
It is thought to constitute a root of origin for the glosso- 
pharyngeal, like the ascending root of the fifth nerve. It has 
received the various names of the slender bundle, the solitary 
bundle, the posterior respiratory bundle. 

Nuclei of the auditory nerve (Figs. 10, n, 13). 

Usually three nuclei are assigned to the auditory nerve : a 
principal or inner nucleus, containing small cells, lying 
immediately under the floor of the fourth ventricle in its 
outer half or two-thirds, and reaching from the level of the 
auditory striae downward upon the outer side of the glosso- 
pharyngeal nucleus ; an outer or superior nucleus, containing 
large cells, occupying the lateral part of the floor of the fourth 
ventricle outside the nucleus of the sixth nerve, and thus at a 
higher level than the principal nucleus. Two tracts of fibres 



INTRODUCTION. 



41 



come from these nuclei, the one (superficial root of the 
auditory) runs round the posterior border of the restiform 
body just below the pons ; the other (deep root) pierces the 
lower border of the pons. The two roots thus encircle the 
restiform body, and between them (or, indeed, partly situated 
on the superficial root) are cells which make up the third or 
accessory nucleus of the nerve. Fibres also connect the 
auditory nerve with the cerebellum. The trunk of the 
auditory enters the internal auditory canal along with the 
facial, and is distributed to the internal ear ; the superficial 



Accessory (vagal) nucleus, 



Trunk of glossopharyn- 
geal. 



Glosso- pharyngeal nucleus 




Pyramidal tract. 
Olivary body. 

Inter-olivary layer. 

Ascending root of fifth. 

Restiform body. 

Auditory stria. 

, Fibres ascending to outer 
auditory nucleus. 

Principal (or inner) auditory nucleus. 

Transverse Section of Medulla, just below Pons, and at Lower Edge of 
Auditory Stride. 



root goes to the cochlea, the deep root to the semicircular 
canals. 

Nucleus of 'the facial (Figs. 10, n). 

This lies deep in the substance of the pons, somewhat to its 
outer side, and thus has a similar position to that of the 
motor nucleus of the vagus and glossopharyngeal (nucleus 
ambiguus). It may be seen in sections through the lower 
part of the pons, and extends upward to the level of the 
greatest breadth of the fourth ventricle. The intra-pontine 
course of the facial is circuitous, just as is its course in the 
petrous bone. From the nucleus fibres pass upward and 
inward, and then transversely outward between the nucleus of 



4? 



NERVOUS DISEASES. 



the sixth and floor of the fourth ventricle (loop of the facial). 
They then pass forward and outward just internal to the 
ascending root of the fifth, and appear on the surface close to 
the lower edge of the pons, between the olive and restiform 
body. The facial trunk accompanies the auditory into the 
internal auditory meatus, a small branch (pars intermedia of 
Wrisberg) connecting the two. It enters next the aqueduct 
of Fallopius, being joined at the upper part of this canal by 
the large superficial petrosal or Vidian nerve (which connects 
it with the spheno-palatine ganglion) and a branch from the 
small superficial petrosal (the communicating nerve between 
the tympanic plexus and otic ganglion). Near the end of the 



Fig. 14. 



Longitudinal fibres of pons 
(pyramidal tract). 



Middle peduncle of cere- 
bellum cut through 



Ascending root of v. 




Transverse fibres of pori 



Fibres of vi. 
Fibres of facial. 



Nucleus of vi. Fibres of facial (ascending bundle). 
Transverse Section of Pons through Eminentia Teres. 



Fallopian aqueduct the facial gives off the chorda tympani, 
which connects it with the lingual nerve, the sub-maxillary 
ganglion, and tongue. 

The facial nerve lies close to the inner wall of the tympanic 
cavity as it passes through the petrous bone ; whereas the 
chorda tympani passes across the cavity between the incus 
and malleus. 

Not far from the facial nucleus, but deeper still in the sub- 
stance of the medulla, is a nucleus known as the superior oliv- 
ary body. 

Nucleus of the sixth nerve (Figs. 10, 11, 14). 

This lies near the middle line, in the upper half of the 



INTRODUCTION. 



43 



fourth ventricle, above the level of the striae acousticse, un- 
derneath a prominence in the funiculus teres, called the emi- 
nentia teres. Around the nucleus curve the fibres of the 
facial, as above described. The fibres of the sixth run 
forward from the nucleus through the pons to its superficial 
origin, which is at the lower border of the pons upon its 
front aspect, in a line with the origin of the hypoglossal. The 
nerve trunk runs forward in the floor of the cavernous sinus, 
and out through the sphenoidal fissure to the external rectus 
muscle of the eye. 

Nucleus of the fifth {trigeminus). (Figs. 10, n, 15.) 
The fifth nerve rises in two divisions : a large sensory divi- 



Fig. 15. 



Longitudinal fibres of 
pons (pyramidal 
tract). 



Middle peduncle of 
cerebellum cut 
through. 



Motor nucleus of v 



Posterior longitud 
nal bundle. 



Transverse fibres of 
pons. 




Part of cerebellum. 
Sensory nucleus of 



Fibres passing from 
v. to middle line. 



Transverse Section of Pons through Origin of sth Nerve (fr, 
lion lent by Dr. Tooth). 



a Prepara- 



tion and a small motor. Of these two the sensory is (at its 
superficial origin) at a rather lower level than the motor. Its 
deep origins areas follows: — 

1. A sensory nucleus beneath the upper and outer part of the 
fourth ventricle. 

2. A descending root, constituted by a band of fibres which 
runs down to the nucleus through the pons from the level of 
the anterior corpora quadrigemina. It probably passes into 
the motor division of the nerve. 

3. An ascending root, a bundle which originates below at 



44 NERVOUS DISEASES. 

the upper part of the tubercle of Rolando, just about the 
junction of the cord and the medulla, and thence runs 
upward to the nucleus, being pierced on its way by the fibres 
of the spinal accessory, pneumogastric, and glosso-pharyngeal. 
It probably connects with the sensory division of the nerve. 

4. A third band of fibres, sometimes called the medial 
root, which runs inward along the floor of the ventricle 
toward the middle line. 

The sensory division of the nerve, passing outward from 
the nucleus, appears at the outer part of the pons, not far 
from its upper border. 

The motor nucleus is placed somewhat deeply beneath the 
floor of the ventricle in its outer part, upon the mesial side 
of the sensory fibres as they pass to their point of exit. The 
motor division of the nerve' at its superficial origin lies at a 
slightly higher level than the sensory, but soon passes beneath 
it. Both divisions pass underneath the dura mater to the 
apex of the petrous bone, where the sensory part is interrupted 
by the Gasserian ganglion, from which spring its three large 
branches, viz. : — 

1. The ophthalmic, which passes forward with the third and 
fourth nerves in the outer wall of the cavernous sinus, and out 
through the sphenoidal fissure. 

2. The superior maxillary, which pierces the sphenoid bone 
at the foramen rotundum, and crossing the spheno-maxillary 
fissure comes out on the face by the infra-orbital foramen. 

3. The inferior maxillary, which passes out by the foramen 
ovale, and is joined by the motor division of the fifth. 

Nucleus of the third and fourth nerves (Figs. 10, 16, 17, 
18). — This lies in the floor of the Sylvian aqueduct, and 
extends from midway between the anterior and posterior 
corpora quadrigemina (this lower part constituting the nucleus 
of the fourth) up to the posterior part of the third ventricle. 
The course of the fibres of the two nerves differs remarkably. 
Those of the fourth run downward and backward into the 



INTRODUCTION. 



45 



valve of Vieussens, decussate here, wind round the superior 
cerebellar peduncles, pass forward in the outer wall of the 
cavernous sinus, leave the skull by the sphenoidal fissure, and 
finally end in either superior oblique muscle. The fibres of the 




Upper part of pons. 



Fillet (medial or superior 
division). 



Superior cerebellar pedun- 
cle. 

Posterior longitudinal bun- 
dle. 
Nucleus of iv. 

Descending root of v. 



Fillet (lateral or inferior 
division). 
Transverse Section of Pons, at Level of Inferior Corpora Quadrigemina. 



third run forward through the crus cerebri, through the " red 
nucleus," and become superficial between the crura cerebri 
just above the pons. The basilar artery separates the nerve 



/ Crusta or pes pedunculi 



Substantia nigra. 



Superior cerebellar peduncle 
(decussating with its fellow). 



Posterior longitudinal bun- 
dle. 



Aqueductus Sylvii. 

Transverse Section through Crura Cerebri, between Superior and Inferior 
Corpora Quadrigemina (from a Preparation lent by Dr. Tooth). 

of the two sides. Each third nerve then travels forward in 
the outer wall of the cavernous sinus, leaves the skull through 
the sphenoidal fissure, and is distributed to the muscles of the 
eyeball and levator palpebrse. 




4 6 



NERVOUS DISEASES. 



In connection with the oculo-motor nuclei may be men- 
tioned the " posterior longitudinal bundle." This is a small 
band of white fibres which runs a little distance below the 
Sylvian aqueduct and the floor of the fourth ventricle, near 
the middle line and parallel with it. It is thought to con- 
nect the nucleus of the third and fourth with that of the 
sixth nerve. Above, it terminates in the gray matter around 
the wall of the third ventricle ; below, it is continuous with 
fibres from the anterior columns of the cord ; according to 
some authorities it is traceable for some way down the cord. 




Crusta or pes pedunculi 



Substantia nigra. 

Red nucleus (nucleus 
tegmenti) pierced by 
fibres of iii. 

Fillet. 

Nucleus of iii. 

Aqueductus Sylvii. 

Transverse Section through Crura Cerebri, at Level of Superior Corpora 
Quadrigemina [from a Preparation lent by Dr. Tooth). 



The optic and olfactory nerves belong to a higher level of 
the brain, but maybe considered here for completeness' sake. 

The optic tract originates from the anterior corpus quadrige- 
minum (the brachium of this body passes almost directly into 
this tract), from the " pulvinar " or posterior part of the optic 
thalamus, and from the external corpus geniculatum.* The 
tracts wind round the crus cerebri of each side and join at the 
optic commissure. Here there is a partial decussation (which 
will be described later), and thus the optic tracts pass into 

* Such fibres as come from the internal corpus geniculatum are said to 
be merely commissural, passing through the optic commissure to the corpus 
of the other side. 




Superficial Origins 
I'. Olfactory tract. 

II. Optic nerve. 
1 1'. Optic tract. 

III. Third or oculo-motor 
nerve. 

IV. Fourth nerve. 

V. Fifth nerve, sensory root. 
V + Fifth nerve, motor root. 
1,2,3. Main divisions of fifth. 

VI. Sixth nerve. 

VII. Facial nerve. 

VIII. Auditory nerve. 

IX. Glosso-pharyngeal. 

X. Vagus. 

XI. Spinal accessory. 



ci CO. 



of Cranial Nerves (/ram 
I XII. Hypoglossal. 
I CI. First cervical nerve. 
! C. Island of Reil. 
\ Th. Optic thalamus (the Is- 
land of Reil having been 
removed). [turn. 

i. Internal corpus genicula- 
c. External geniculatum. 
h. Pituitary body. 
tc. Tuber cinereum. 
a. One of the corpora albi- 

cantia. 
Sy. Sylvian fissure, 
xx Anterior perforated 
space. 



Quain's "Anatomy"). 

x Posterior perforated 

space. 
P. Cerebral peduncle. 
PV. Pons Varolii. 
Ce Cerebellum. 
/. Fillet. 
Jl. Flocculus. 
pa. Anterior pyramid. 
o. Olive. 
d. Anterior median fissure 

of cord. 
V. Lateral tract of medulla. 
Ca. Anterior column. 
CI. Lateral column. 



47 



48 NERVOUS DISEASES. 

the optic nerves, which run through the foramina optica to 
the back of the eyeballs. 

The ulterior destination of the optic tracts (on the side of 
the cerebral hemispheres) is to the cortex of the occipital 
lobe, which it reaches via the posterior part of the internal 
capsule, and the fibres which radiate therefrom to the cortex. 

The olfactory nerve consists of the olfactory bulb and olfac- 
tory tract, and is regarded rather as a lobe of the brain than 
as a distinct nerve. The bulb lies on the upper surface of the 
ethmoid, through which fibres pass to the nasal fossa. The 
tract as it runs backward bifurcates, the one division or root 
goes toward the Sylvian fissure, the other toward the longi- 
tudinal fissure. The first of these divisions probably goes to 
the tip of the temporo-sphenoidal lobe and the gyrus uncinatus. 

Region of Crura Cerebri. — Each crus cerebri connects 
its own hemisphere with the cerebellum behind and the pons 
and medulla below. The two crura are fused as they approach 
the pons, and thus roof in the open space of the fourth ventri- 
cle, so as to form the aqueduct of Sylvius or iter a tertio ad 
quartum ventriculum. This region is surmounted by the two 
pairs of ganglia called the corpora quadrigemina. Deeper 
down in each crus is placed another ganglion, called the red 
nucleus. Just below the Sylvian aqueduct lie the nuclei of the 
oculo-motor nerves. 

In a transverse section through the crura (Fig. 9C, 17, 18) 
the division into ventral and dorsal parts — called respectively 
the crusta and the tegmentum — is marked, as we have said, 
by a layer of darkly pigmented cells called the substantia 
nigra. 

The crusta — /'. e., the ventral or lower part — consists of the 
following tracts of fibres (Fig. 9 c) : — 

(a) In its middle third, the pyramidal or motor tract, 
descending from the motor area of the cerebral cortex, via the 
posterior limb of the internal capsule to the medulla and 
cord. 



INTRODUCTION. 49 

(/?) In its internal third (J. e., between the pyramidal tract 
and the middle line) a tract of fibres which descend from the 
cortex in front of the motor area (prefrontal region), via the 
anterior limb of the internal capsule, to the pons and thence 
to the cerebellum (fronto-cerebellar fibres). 

(j) In its external third fibres which descend from the 
cortex of the temporo-sphenoidal and occipital lobes, which 
have the same destination as the last set, but which have not 
(according to Flechsig) any place in the internal capsule 
(temporo-occipital cerebellar fibres).* 

The tegmentum (Fig. 9 c, 16-18) is a more complicated 
region. It is surmounted, as just mentioned, by the anterior 
and posterior corpora quadrigemina. Each of these bodies, 
anterior and posterior, sends forward a brachium or tract of 
fibres which runs to that part of the optic thalamus from 
which the optic tract springs ; indeed, the brachium of the 
corpus quadrigeminum anterius is almost continuous with the 
optic tract. The corpora quadrigemina receive fibres from 
the fillet and from the reticular formation behind them. 
Probably they are also connected with the underlying oculo- 
motor nuclei. Their functions are still imperfectly known. 

Beneath them, on section through the tegmentum, we find 
the Sylvian aqueduct, or iter a tertio ad quartum ventriculum, 
and around it. 

* These are the three principal divisions of the crusta, but there are sun- 
dry smaller divisions as follows : — 

S. The inner part of the motor tract, that which lies next to the fronto- 
cerebellar fibres, is sometimes called the " geniculate " tract, because it 
contains the fibres which come from the genu or knee of the internal cap- 
sule; these are destined for the face and tongue (bulbar nuclei), whereas 
the bulk of the motor tract goes to the limbs. 

f.. Deeply placed between the three main tracts and the substantia nigra 
are fibres which are supposed to run from the caudate nucleus to the pons, 
and thence to the cerebellum (like the fronto-cerebellar and temporo- 
occipital cerebellar fibres). 

£. Fibres which connect the crusta with the fillet. 



50 NERVOUS DISEASES. 

a. Gray matter, part of which constitutes the nuclei of the 
third and fourth cranial nerves. 

ft. On either side, the small band of fibres which forms the 
descending root of the fifth nerve. 

y. Ventrally upon either side the posterior longitudinal 
bundle. 

The main mass of the white substance of the tegmentum 
consists, however, of the superior cerebellar peduncles and the 
fillets of either side. The position of these varies according 
to the level at which the section is taken. 

Thus, at the lowest level of this region (viz., at the junction 
of the pons and crura) each superior cerebellar peduncle on 
its way up from the corresponding side of the cerebellum is 
placed at the dorsal and lateral part of the section ; but as it 
ascends brainward, it tends to the deeper part and toward the 
middle line (Fig. 16), and reaching this it crosses over and 
decussates with its fellow (Fig. 17) (at a level midway between 
the superior and inferior corpora quadrigemina), and finally 
terminates (at the upper level of the superior corpus quadri- 
geminum) in a large round nucleus, called, from its color, the 
red nucleus, or nucleus tegmenti (Fig. 18). This nucleus is 
pierced by the arching fibres of the third nerve, and forms a 
prominent object in a section at the upper part of the crura 
cerebri. It probably sends fibres upward to the optic thalamus 
and lenticular nucleus. 

Meanwhile the fillet, which at the upper part of the pons 
(Fig. 15) lay deeply between the dorsal and ventral portions 
of the nervous axis, splits up (as we have already said). Its 
lateral or inferior portion becomes superficial to the superior 
cerebellar peduncle as this tracks inward, and winds round 
its outer edge to gain the inferior corpus quadrigeminum 
(Fig 16) ; its mesial or superior portion passes mainly to the 
superior corpus quadrigeminum and to the optic thalamus, 
while a small part joins the crusta of the cerebral peduncle. 

Cerebellum. — The cerebellum is an organ of peculiar 



INTRODUCTION. 



51 




52 NERVOUS DISEASES. 

structure as regards its minute anatomy. Its cortical sub- 
stance differs singularly from that of the cerebrum, being 
characterized by the single layer of the large "cells of 
Purkinje," and the thickly set layer of granules, reminding 
us of those in the retina. The organ has two lateral lobes 
and a middle lobe or " vermis." Deeply placed in the white 
matter of each lateral lobe is a nucleus, consisting of a wavy 
capsule of gray matter, not unlike the olivary body, and called 
the dentate nucleus. In the middle lobe are nuclei known as 
"roof nuclei " (nucleus fastigii), because they lie in that part 
which roofs in the fourth ventricle. 

The functions of the cerebellum are incompletely known. 
There is reason to think that the division into lateral and 
middle lobes corresponds to difference in function ; and that 
the particular function commonly ascribed to the cerebellum 
— viz., the co-ordination of muscular movement required for 
balancing the body, is limited to the middle lobe. 

At any rate, the connections of the cortex of the lateral 
hemispheres, of the nucleus dentatum of the lateral hemisphere, 
and of the middle lobe are different. They are illustrated in 
the diagram, and they are mainly as follows: — 

Middle Lobe (vermis). — In the cortex of this lobe terminate 
the direct cerebellar tracts, which ascend from the cord, via 
the inferior cerebellar peduncles (restiform bodies).* Other 
fibres (not all shown in the diagram) are said to pass, via the 
restiform bodies, to the middle lobe — (i) from the formatio 
reticularis of the medulla; (2) from the auditory nuclei; (3) 
from the nuclei of the posterior pyramids of both sides. f 
The dentate nucleus of each lateral hemisphere is joined below 
to the olivary body of the opposite side by fibres which run 

* Whether they decussate, as represented in the diagram, or no, is a little 
uncertain. 

f Should be represented in the diagram as going to the middle (not 
lateral) cerebellar lobe. 



INTRODUCTION. 53 

in the inferior cerebellar peduncle. Upward from the dentate 
body run fibres which form the bulk of the superior cerebellar 
peduncle ; this peduncle, at first placed superficially at the 
dorsum and side of the pons, soon dips inward, decussates 
with its fellow in the middle line, and passes into the opposite 
red nucleus. From the red nucleus arise fibres (not marked 
in the diagram) which pass upward probably to the lenticular 
nucleus and region of the optic thalamus (either into the 
thalamus itself or through it to the sensory area of the cerebral 
cortex). 

The cortex of each lateral cerebellar hemisphere sends fibres 
to its own dentate nucleus. It is also connected with the 
opposite cerebral hemisphere in the following way {vide Fig. 
9 c, and p. 49) : — 

(1) Fibres from the frontal lobe of the cerebrum descend 
through the internal capsule (anterior limb) and cms cerebri 
(internal third of the crusta) to the pons; crossing to the 
opposite side of the pons, they terminate in the cells scattered 
amongst its transverse fibres.* From these cells other fibres 
arise, which run via the middle cerebellar peduncle to the 
cortex of the corresponding cerebellar hemisphere. 

(2) Fibres from the temporo-sphenoidal and occipital lobes 
of the cerebrum descend in a similar way through the external 
third of the crusta (apparently missing the internal capsule) 
to the pons and thence to the cerebellum. 

(3) Fibres from the caudate nucleus, deeply situated in the 
crusta, establish a like connection with the pons and cere- 
bellum. 

These connections are crossed, it will be noticed ; each 
lateral lobe of the cerebellum is joined to the opposite cere- 
bral hemisphere, the opposite side of the spinal cord, and the 
opposite olive. Atrophy (or non-development) of one cere- 

* Should be represented in the diagram as connecting with cells on the 
opposite side of the pons. 

5 



54 



NERVOUS DISEASES. 




* This and the following diagrams of the cerebrum are on the model of 
the " Clinical Figures " published by Messrs. Daniellsen. 



INTRODUCTION. 55 

bral hemisphere is associated with atrophy of the other half 
of the cerebellum. Similarly, atrophy of one cerebellar hemi- 
sphere is associated with atrophy of the opposite olivary body. 
Cerebral Hemispheres: Their Surface or Cortex. 
— Cerebral convolutions. — The cerebral convolutions, with 
the fissures and sulci which divide them, are indicated on the 
accompanying diagrams. Their arrangement is sufficiently 
constant to allow of diagrammatic representation ; but every 
opportunity should be taken of studying them in nature, for 




Diagram of Upper Surface of Cerebral Hemispheres. 

the subdivision of the convolutions by subsidiary sulci, and 
the frequent slight variation of them, render their identifica- 
tion much more difficult than might be imagined. 

Next to the longitudinal fissure, which receives the falx 
cerebri, and divides the two hemispheres from each other, the 
most important fissures are : — 

The fissure of Rolando, which separates the frontal lobe in 
front from the parietal lobe behind, and upon either side of 
which are ranged the motor convolutions. 



56 NERVOUS DISEASES. 

The fissure of Sylvius, which separates the temporo- 
sphenoidal lobe below from the frontal and parietal lobes 
above. It begins as a wide-lipped opening below, and divides 
into a long horizontal branch and a short vertical one. 

The parieto-occipital fissure, seen upon the inner surface 
of the hemisphere, which separates the occipitallo be behind 
and below from the parietal. 

Taking first the outer and upper aspect of the hemispheres 
(Figs. 21 and 22), we find on either side of the fissure of 
Rolando two parallel convolutions — viz., the ascending fron- 
tal and ascending parietal. The ascending frontal is sepa- 
rated by an interrupted sulcus (praecentral sulcus) from the 
three other frontal convolutions which run horizontally. 
These are called in order from above downward — the first, 
or superior frontal ; the second, or middle ; the third, or 
inferior. The third frontal curves round the vertical branch 
of the Sylvian fissure, merging into the lower end of the 
ascending frontal. (The region where they join is some- 
times called the operculum ; it covers in the island of Reil 
below.) 

The ascending parietal merges at its upper end into the 
superior parietal lobule, which occupies the upper part of the 
parietal lobe. A sulcus, partly horizontal and partly vertical 
in direction (intra-parietal sulcus), divides the superior pari- 
etal lobule above, and the ascending parietal convolution in 
front, from the remainder of the lobe. This remainder, 
which is sometimes called the inferior parietal lobule, con- 
tains the supra-marginal gyrus, which bends round the ex- 
tremity of the posterior branch of the Sylvian fissure, and the 
angular gyrus,* which similarly bends round the end of the 



* The term angular gyrus needs an authoritative definition. It is some- 
times used to denote the convolution which curves round the end of the 
parallel sulcus (as in text), sometimes made to include more or less of 
the space between the parallel sulcus and the termination of the Sylvian 



INTRODUCTION. 57 

next principal sulcus — viz., the superior temporo-sphenoidal 
or parallel sulcus. 

Beneath the horizontal part of the fissure of Sylvius lies 
the temporo-sphenoidal lobe, which contains on its outer 
aspect three horizontal convolutions (superior, middle, infe- 
rior). A long sulcus (superior temporo-sphenoidal or parallel 
sulcus) separates the first or superior from the second or 
middle convolution. It runs back till terminated by the 
angular gyrus. 

Behind the parietal and the temporo-sphenoidal lobes lies 
the occipital lobe. The line of demarcation is indefinite, 
being taken as the line which would be marked out by the 
parieto-occipital fissure if prolonged over the outer aspect of 
the brain. In monkeys this fissure actually does reach over 
the external aspect of the brain, but not in man. 

Three occipital convolutions are described — superior, mid- 
dle and inferior. They are joined to the parts in front by 
" annectant " gyri. 

On separating the lips of the Sylvian fissure, there are seen 
the convolutions of the island of Reil (not shown in the 
diagrams.) 

The convolutions upon the inner and lower aspects of the 
brain (Figs. 23 and 24) are more simple. 

Immediately above the corpus callosum (the large commis- 
sure which connects the two hemispheres) lies the gyrus 
fornicatus. This runs parallel to the whole length of the 
corpus callosum, and then curves down behind it, to merge 
in the uncinate convolution. Parallel with the gyrus forni- 
catus and next above it, is the marginal convolution ; the 
calloso-marginal fissure separates the two. Posteriorly, the 



fissure, sometimes even to include what in the text is called supra-marginal 
gyrus. The distance between the ends of the parallel sulcus and the 
Sylvian fissure is variable in the human brain ; in the monkey the parallel 
sulcus joins the Sylvian fissure. 



58 



NERVOUS DISEASES. 



fissure turns up toward the upper aspect of the brain, and thus 
terminates the marginal convolution. The greater part ot 
this convolution corresponds to the superior or first frontal 
convolution on the outer aspect of the brain. But its posterior 
part corresponds to the upper ends of the ascending frontal 
and parietal convolutions, and this part is called the para- 
central lobule. Behind this comes a roughly quadrangular 
area, corresponding to the superior parietal lobe externally. 
It is called the praecuneus or quadrate lobule. It is termi- 



Fig. 23. 
Calloso-marginal fissure. 




Dentate 
fissure (or 
sulcus 
hippocampi) 

Diagram of the Mesial Aspect of the Right Cerebral Hemisphere. 



nated posteriorly by the parieto-occipital fissure, behind and 
below which the occipital lobe begins. The parietooccipital 
fissure runs downward and forward, and receives from behind 
a tributary running horizontally — viz., the calcarine fissure. 
These two mark off a triangular tract called the cuneus. 
Below the calcarine fissure, and reaching forward along the 
under surface of the temporo sphenoidal lobe, are the temporo- 
occipital convolutions. The first, or superior, begins beneath 
the calcarine fissure, where it is also called the lingual lobule, 
and fusing with the end of the gyrus fornicatus forms the gyrus 



INTRODUCTION. 59 

hippocampi or uncinate convolution, which borders and 
extends round the end of the dentate fissure, where it is called 
the uncus (subiculum cornu Ammonis). The dentate fissure 
corresponds to the elevation of the hippocampus major within 
the descending horn of the lateral ventricle ; therefore it is 
also called the sulcus hippocampi. Within it lies the margin 
where the gray cortical matter of the brain terminates, called 
the dentate convolution, or fascia dentata. The second 
temporo-occipital convolution, also called the fusiform lobule, 




Collateral fissure 
Calcarine fissure 

Diagk 

runs parallel to the first, along the inferior aspect of the brain. 
The collateral fissure separates the two. The next convolution 
upon the outer side of this is the third or inferior temporo- 
sphenoidal. 

Functions of Special Parts. — The anatomy of the cere- 
bral convolutions derives its importance from the fact that the 
brain is not (like such organs as the liver) functionally homo- 
geneous, but that each part of the cortex has special functions 
assigned to it. Such a "localization of function" in the 



60 NERVOUS DISEASES. 

brain is now denied by few, although the details of the theory 
are not completely known. 

Motor " Centres." — The function of voluntary move- 
ment is the easiest of investigation, and it is concerning the 
localization of this that we have the most certain knowledge. 
Experiments on animals and observation of disease in man have 
shown certain parts of the brain to have a special connection with 
voluntary movements of the several parts of the body, limbs, 
face, head, and eyes, etc., so that when these parts of the brain 
are stimulated such movements are produced ; and when they 
are destroyed such movements become impossible. These 
parts of the cortex are therefore called the " motor area " ; 
because the net result of activity in this area is movement, 
though what is the intimate nature of the cerebral processes we 
do not precisely know. Roughly speaking, the motor area 
consists of the parts near the fissure of Rolando, but it also 
extends on to the mesial aspect of the brain. Further, it can 
be parceled out into smaller areas, which correspond to move- 
ments of particular limbs, and even of particular segments of 
them ; these smaller areas are called the " motor centres " for 
the arm, leg, face, etc. 

The ascending frontal and parietal convolutions are occu- 
pied by the centres for the face, arm and leg (Fig. 25) — in 
that order from below upward ; each centre occupying 
(roughly speaking) a third of the whole length of the convolu- 
tions. There is no strict line of demarcation between them, 
but it has been possible by experiments on monkeys to map 
them out fairly, and even to find the points corresponding to 
the several segments of the limbs, and particularly of the 
thumb, fingers, hallux, etc. Rare cases of limited disease 
have sometimes allowed a similar minute localization in man. 

The face centre occupies the lower ends of the two ascend- 
ing convolutions. It is limited above (Horsley) by a line 
drawn forward from the lower end of the intra-parietal sulcus 
parallel with the horizontal branch of the Sylvian fissure. In 



INTRODUCTION. 



6l 



its upper part are probably represented movements of the 
upper part of the face, and in its lower part movements of the 
lower face, lips, tongue and vocal cords.* The posterior part 
of the third frontal convolution on the left side constitutes 
" Broca's convolution." Destruction of this part produces 
that condition of speechlessness which is commonly called 
aphasia. 

The arm centre occupies the middle part of the central 
convolutions, but it probably runs forward and upward into 

Fig. 25. 




Diagram op Motor and Sensory Centres on External Surface of 
Left Cerebral Hemisphere. 



the posterior part of the superior frontal (here blending with 
the centre for the leg), and to the mesial aspect of the brain. 



* Spasm of the angle of the mouth (zygomatici) was in one case depend- 
ent on a lesion of the ascending frontal just opposite the origin of the 
sulcus separating the 2d and 3d frontal convolution (Berkeley). 

Adduction of the vocal cords (Ilorsley and Semon) is represented in the 
monkey at a point just posterior to the lower end of the prcecentral sulcus 
— i.e., in the ascending frontal at the level of the 3d frontal. There is 
no centre for abduction of the cords. 
6 



62 NERVOUS DISEASES. 

The particular parts of the arm are said to be represented in 
the following order from above downward — shoulder, elbow, 
wrist, fingers, thumb. Movements of the thumb appear to be 
represented at the lowest and most posterior part of the cen- 
tre, just in front of the lower end of the intra-parietal sulcus, 
and of the fingers just above and in front of this. The posi- 
tion of the centre for these parts is important because con- 
volutions frequently commence in them. 

The leg centre is at the highest part of the ascending frontal 
and parietal, probably not reaching down as far as the level 




Tactile sense. 
Diagram of Motor and Sensory Centres on Mesial Aspect 
of Left Cerebral Hemisphere.* 

of the superior frontal sulcus (Govvers), and extending to un- 
certain limits anteriorly and posteriorly. On the mesial 
aspect of the brain it occupies the paracentral lobule. Move- 
ments of the hallux are specially represented at a point just 
in front of the highest part of the fissure of Rolando. 

To complete this account of the motor area on the ex- 
ternal aspect of the brain it should be said that there is in 
the monkey, and probably in man also, a largish area cover- 
ing the posterior parts of the horizontal frontal convolutions, 

* The centre for touch should probably extend much further forward 
along the gyrus fornicatus. ( Vide Savill, Brain, 1891.) 



INTRODUCTION. 63 

wherein are represented sideward movements of the head and 
eyes. 

The motor area extends also on to the mesial aspect of the 
hemispheres (Fig. 26). The marginal convolution in monkeys 
(Horsley and Schafer) contains motor centres, which may be 
enumerated in the following order from before backward : — 

1. For the head and eyes (a very small area). 

2. For the upper limb (viz., forearm and hand, shoulder). 

3. For the trunk (upper part, pelvic part). 

4. For the lower limb (viz., hip, knee, foot, toes). 

The areas 1, 2, 4 are continuous with those for head, arm, 
and leg on the external aspect of the hemisphere. The centre 
for the trunk is almost entirely upon the mesial aspect. As 
might be expected, the centres for shoulder and hip are 
grouped on either side of the trunk centre. 

In man we may surmise that the region of the paracentral 
lobule completes the centre for the lower limb, and that in 
front of this may lie centres for the trunk, shoulder, head and 
neck. 

Sensory "Centres." — By sensory centres we mean those 
areas of the cortex, stimulation of which gives rise to sensa- 
tions, such as those of sight, hearing, and the like, and destruc- 
tion of which causes a corresponding disability of sensation 
— e. g., blindness, deafness, etc. Concerning the position of 
these centres we know less than of the motor. The centre 
for vision was originally placed by Ferrier in the angular 
gyrus,* destruction of this part produced loss or impairment 
of vision in the opposite eye (crossed amblyopia). Others, as 
Munk, placed the visual centre in the occipital lobes, the 
relation being such that destruction of one (say the right) 
occipital lobe produced blindness in the opposite (left) half 
of the field of vision in both eyes (crossed hemianopia). As 



* Extending also to the supra-marginal convolution : vide diagram in 
Ferrier's " Functions of the Brain," ed. 2, p. 478. 



64 NERVOUS DISEASES. 

regards man there are facts in favor of both these views, and it 
may be that they are both true, the occipital lobe constituting 
a centre for the opposite half-field of vision, the angular gyrus 
for the vision of the opposite eye.* The centre for hearing 
is commonly placed in the posterior part of the superior tem- 
poro-sphenoidal convolution : but this is disputed by some 
authorities. 

The centre for smell is placed at the tip of the mesial aspect 
of the temporo-sphenoidal lobe (region of the uncus) ; and 
that for taste is probably in the same neighborhood. 

Cutaneous sensation is thought to be localized in the unci- 
nate gyrus and its continuation, the gyrus fornicatus — parts 
which as a whole have been called the falciform or limbic 
lobe. 

White Matter of Cerebral Hemispheres. — The inte- 
rior of the hemispheres consists partly of white matter, partly 
of the gray masses known as the basic ganglia (corpus striatum 
and optic thalamus). 

The white matter, which we will consider first, serves 
solely to establish paths of connection between the cortex, 
the ganglia, and other parts. These connecting fibres are 
classified into (1) Commissural fibres, passing from hemisphere 
to hemisphere, which chiefly run in the corpus callosum and 
commissure of the third ventricle. (2) Longitudinal or 
"collateral" fibres, which connect different parts of the 
cortex of the same hemisphere, and which run partly in the 
fornix, gyrus fornicatus, and other structures, partly imme- 
diately beneath the cortex, where they are known as " associa- 
tion fibres." (3) Peduncular fibres, which pass from the 
cortex to the crura or peduncles of the brain, and thence to the 
pons, cerebellum, and spinal cord. To these must be added 
fibres which connect the basic ganglia with the peduncles 
below, or with the cortex above. 

* And probably in a less degree for the eye of the same side also. 



INTRODUCTION. 



65 



Of these sets the peduncular fibres are the best known. 
They converge from all parts of the cortex, forming thus 
what is known as the corona radiata, till they are collected 
together into a flat band, called "the internal capsule." 
This important structure is shown as cut transversely in the 
horizontal section figured in Fig. 27. It lies between the 




Caudate nucleus 
(tail of). 

Posterior horn of 

lateral ventricle. 
Diagram to show the Parts Exposed by a Horizontal Section through 
Hemispheres, at the Level of the Basic Ganglia. 



lenticular nucleus, on its outer side, and the caudate nucleus 
and optic thalamus on its inner side. It has, in this section, 
the shape of a V, with its apex pointing to the middle line 
and its limbs spread out to an obtuse angle. There is thus an 
anterior and a posterior limb or division in the capsule, and 
their point of junction, apex of the V, is called its genu or 



66 



NERVOUS DISEASES. 



knee. The fibres in its anterior limb come from the cortex 
in front of the motor area (prefrontal area), and descend, as 
mentioned above (p. 49, ,?, and p. 53, 1), through the crusta 
of the cerebral peduncle to the pons and opposite lobe of 
the cerebellum. The genu and anterior two-thirds of the 
posterior limb of the capsule are occupied by fibres which 
descend from the motor area of the cortex to the spinal cord. 
In the capsule these motor fibres are arranged in a certain 
order from before backward, roughly speaking, thus : those 




Transverse Vertical Sections (diagrammatic) through the Cerebral 

Hemispheres. 

A. Through the posterior part of the horizontal frontal convolutions (pediculo-frontal 

section of Pitres). 

for the face, tongue, etc., at the genu, then those for the 
upper limb, and then those for the lower ; * so that what is 



* Beevor and Horsley, in experiments on monkeys, found that the fibres 
had the following relative position from before backward : — 
(1) Fibres for movement of the eyes. 



[2) 

(3) 
(4) 
(5) 
(6) 



head. 

tongue. 

mouth. 

upper limb. 

lower limb : hip, knee, toes. 



INTRODUCTION. 



6 7 



inferior in the cortex is anterior in the capsule. The remaining 
(posterior) third of the capsule consists of fibres going up- 
ward to the sensory parts of the cortex. 

The general direction of the fibres of the internal capsule 
— viz., as a tract which connects the corona radiata above 
with the crura cerebri below, is shown better in vertical sec- 
tions (Figs. 28 b, 28 c). 

Further back than the internal capsule, curving round the 




Nucleu 
amygdala 



Internal capsule. 
Through the Ascending Frontal Convolution (Frontal Section of Pitres). 



posterior horn of the lateral ventricle, toward the occipital 
cortex, is a tract of fibres known as the optic radiations. It 
connects the cortical centre for vision with the termination 
of the optic tract below (p. 48). 

The upper surfaces of the large basic ganglia — viz., the 
corpus striatum and optic thalamus, are seen as soon as 
the ventricles are exposed from above. For further exam- 
ination the horizontal and vertical sections (Figs. 27 and 28) 



68 



NERVOUS DISEASES. 



may be used. The so-called corpus striatum consists of two 
parts, caudate nucleus and lenticular nucleus. The caudate 
nucleus is the only one that appears in the floor of the 
ventricle. The main part of this lies anteriorly, and is 
separated from the lenticular nucleus by the anterior limb of 
the internal capsule. But it sends a long tail or cauda 
backward, which arches over the optic thalamus and curves 
downward so as to appear in the wall of the descending 



Caudate nucleus. 
Island of Reil. 

Claustrum. 



Lenticular nu- 
cleus. 

External cap 

sule. 

Descending cor- — .— 
nu of lateral 
ventricle. 

Dentate fissure — 
(or sulcus hip- 
pocampi.) 




Internal capsule 



C. Through the Ascending Parietal Convolution (Parietal Section of Pitres). 



cornu of the lateral ventricle. At its anterior part the caudate 
nucleus is partly fused with the lenticular nucleus. 

The lenticular nucleus, placed externally, fills up the 
angle made by the diverging limbs of the internal capsule ; 
the posterior limb of the capsule separates it from the optic 
thalamus and the anterior limb separates it from the caudate 
nucleus. The inner part of the lenticular nucleus is less dark 
than the outer, and by some authors is called the "globus 
pallidus;" the outer part is called the "putamen." The 
caudate nucleus (like the prefrontal cortex) is connected to 



INTRODUCTION. 



6 9 



the pons, and ultimately to the cerebellum, by fibres which 
descend through the crusta of the cerebral peduncle {vide p. 
53, 3, and foot-note to p. 49, e). To the lenticular nucleus, 
or at least to the globus pallidus, runs a band of fibres from 
the tegmentum of the peduncle. This band is called the 
lenticular loop. It goes transversely across the internal cap- 
sule and underneath the optic thalamus, and connects the 
lenticular nucleus with the red nucleus and superior cerebellar 
peduncle, and also with the fillet. 



Caudate nucleus. 



Descending cor- 
nu of lateral 
ventricle 

Dentate fissure 
(or sulcus hip- 
pocampi). 




D. Thr 



jgh_the Supra-marginal Gyrus and Superior Parietal Lobule (Pedi 
parietal Section of Pitres). 



The optic thalamus is extensively connected above with 
all parts of the cerebral cortex by fibres which spread out in 
the corona radiata; fibres also run in the fornix, which con- 
nect it with the hippocampal gyrus or uncinate convolution. 
The posterior extremity of the thalamus is called the " pul- 
vinar." It exhibits the two eminences known as the external 
and internal corpus geniculatum (Fig. 19). This region is 
important as constituting the origin of the optic tracts. Upon 
the side of the cerebral peduncles the optic thalamus is con- 



JO NERVOUS DISEASES. 

nected chiefly to the tegmentum — viz., to the red nucleus and 
superior cerebellar peduncle, brachia of corpora quadrigemina, 
reticular formation and fillet (?). 

The functions of the basic ganglia are still doubtful. 
Till recently it was thought that they were placed — the corpus 
striatum upon the path of the efferent fibres from the cortex, 
the optic thalamus upon the path of the afferent fibres ; so that 
motor impulses underwent some modification in the corpus 
striatum, and sensory impulses in the optic thalamus. But 
we know now that a large bulk of motor fibres proceed 
straight downward from the cortex, via the internal capsule, 
to the pons and cord, without any interruption in the corpus 
striatum. Very probably sensory fibres ascend in the same 
way, without interruption in the optic thalamus. It has been 
suggested that the caudate nucleus and the external part at 
least of the lenticular nucleus are really infolded portions of 
the cortical gray matter. As to the optic thalamus, the 
connection of its "pulvinar" with one important sense, that 
of sight, cannot be denied ; but the function of the remainder 
is doubtful. 

External Capsule ; Claustrum, etc. — Before leaving 
these regions, we may add, to complete the description of 
Figs. 27 and 28, that the layer of white matter just outside 
the lenticular nucleus is called the external capsule. Its 
function is not known. Outside this, again, is a thin layer 
of gray matter known as the "claustrum," also of unknown 
function, but supposed by some to be essentially part of the 
gray matter of the island of Reil, under which it lies. 
. Vessels of Cerebrum.— The vascular supply of the 
cerebrum is important, because some of the commonest 
cerebral diseases originate primarily in the vessels and not in 
the nerve-tissue, and therefore the distribution of the disease 
follows the distribution of the vessels. The arteries of the 
cerebrum all spring from the circle of Willis, that is, from the 
well-known arterial ring formed at the base of the brain by 



INTRODUCTION. J I 

the communications between the basilar artery behind and 
the two internal carotids laterally. The trunks which arise 
from the circle of Willis are the two anterior cerebral arteries, 
which run on the inner aspect of either frontal lobe in the 
longitudinal fissure ; the two middle cerebrals, which are 
practically continuations of the carotid trunks, running in 
the fissures of Sylvius ; and the posterior cerebrals, which wind 
backward and outward over the crura cerebri to the occipital 
lobes. These main trunks are distributed in two ways — (i) By 
"cortical" branches, which ramify in the meninges and are 
distributed to the cortex and subjacent white matter ; (2) By 
"central" arteries, small twigs which pierce the base of the 
brain directly and are distributed to the large ganglia and 
their neighborhood. These central arteries form no anasto- 
moses ; hence occlusion of any such artery is followed by 
softening of all the brain-district supplied by it. Whether 
the cortical arteries anastomose is uncertain ; but at least their 
anastomoses, if such exist, are not so large and regular as those 
in other parts of the body. 

The central distribution of the anterior cerebral is small, 
taking in only the head of the caudate nucleus. That of the 
posterior cerebral includes the crus cerebri, choroid plexus, 
and posterior part of the optic thalamus and internal capsule. 
That of the middle cerebral is most important, for this artery 
supplies the corpus striatum (except the anterior part of the 
caudate nucleus), the optic thalamus and internal capsule 
(except their posterior extremities). This is effected by two 
sets of branches — (a) small twigs which run straight up from 
near the origin of the middle cerebral, (/?) larger branches 
which course outward in the external capsule, skirting the 
lenticular nucleus. One of these latter, from its great liability 
to give way in disease, has been called by Charcot the 
"artery of cerebral hemorrhage." 

The cortical distribution of the three arterial trunks is 
represented in Figs. 29 and 30. 



72 



NERVOUS DISEASES. 



Externally, the branches of the middle cerebral cover the 
largest area — viz., the ascending frontal and parietal convolu- 
tions (except the upper part of the former), the roots of 

Fig. 29. 




Distribution of Arteries on External Surface of Cerebral Hemisphere. 

the middle and inferior frontal, the superior and inferior 
parietal lobules, the upper two temporo-sphenoidal convolu- 




Distribution of Arteries on Mesial Surface of Cerebral Hemisphere. 



tions, and the island of Reil. That is to say, the whole 
external motor area (except part of the lower limb centre) 



INTRODUCTION. 73 

and the speech centre on the left side, and a large part of the 
supposed sensory area (auditory and angular). The rest of 
the temporo-sphenoidal lobe and- the occipital lobe are 
supplied by the posterior cerebral ; the anterior and upper 
parts of the frontal lobe by the anterior cerebral. 

On the mesial surface the conditions are reversed, for the 
middle cerebral supplies none of this surface ; it is divided 
between the other two arteries ; the posterior cerebral supplies 
the occipital ("half-vision" centre) and temporo-sphenoidal 
convolutions; the anterior cerebral all the convolutions in 
front of this, embracing therefore the motor area of the 
mesial surface. 

Relations of Cerebral Convolutions to Points on 
Surface of Skull. — The anatomical relations of the several 
convolutions and fissures to the external surface of the skull 
must be studied with exactitude by surgeons who engage in 
operations on the brain. 

The simplest rules upon this subject are those given by 
Hare, and it may be sufficient to repeat them here. 

The glabella is the root of the nose in the middle line 
opposite the upper border of the orbits. 

The inion is the external occipital protuberance. A line 
drawn from glabella to inion through the vertex is called the 
sagittal line. It corresponds to the longitudinal fissure. Its 
length is from n to 13 inches, as a rule. Its middle point is 
called the mid-sagittal point. 

Half an inch (Thane) or three-quarters of an inch 
(Makins) behind the mid-sagittal point lies the upper end 
of the fissure of Rolando, or, strictly speaking, the point 
where this fissure, if prolonged, would cut the longitudinal 
fissure. The direction of the fissure of Rolando is downward 
and forward, so as to form an angle of 67 with the sagittal 
line. This may be conveniently marked upon the skull by 
Horsley's method. Two strips of soft metal are joined so as to 
make the required angle ; they are then moulded to the skull, 



74 NERVOUS DISEASES. 

with the inner border of one along the sagittal line and the 
angle y 2 or ^ inch behind the mid-sagittal point ; then the 
inner border of the other will correspond to the fissure of 
Rolando. 

The fissure of Sylvius is found by drawing a line back- 
ward from the external angular process of the frontal bone 
backward to the external occipital protuberance, and marking 
a point on it i}i inch from the external angular process. 
This point marks the origin of the fissure, and a line drawn 
from it to the centre of the parietal eminence marks the 
course of its horizontal branch. 

The parieto-occipital fissure is two inches behind the upper 
end of the fissure of Rolando. 



CHAPTER II. 
MORBID ANATOMY OF NERVOUS SYSTEM. 

We shall endeavor in this chapter to give a short account 
of the commonest morbid processes which affect the nervous 
system, limiting ourselves to those which produce definite 
anatomical changes. 

Such diseases may either (i) arise primarily in the nerve 
elements or parenchyma, or (2) may begin in its envelops, 
vessels, or interstitial tissue, the nervous tissue suffering sec- 
ondarily. 

DISEASE OF NERVOUS PARENCHYMA. 

Primary parenchymatous disease is perhaps the least com- 
mon of the two. It may be either inflammatory or degenera- 
tive. The line between the two classes cannot always be 
drawn. 

Acute Inflammation and its Results. — Acute inflam- 
mation of nerve-tissue is more easily recognized by its results 
than during the early stages of the process. In the brain we 
may perhaps take as evidence of inflammatory hyperaemia a 
general pink suffusion or discoloration, with numerous and 
well-marked " puncta cruenta." Mere fullness of the menin- 
geal veins, particularly if limited to the posterior part of the 
head, is no criterion, since it may depend on post-mortem 
gravitation of the blood. 

Cerebral Softening. — But the first result of inflammation 

— viz., softening — has more definite characters. The tissue 

has a reddish color, from the admixture of blood and blood 

pigment, the contour of white and gray matter is ill-defined, 

75 



y6 NERVOUS DISEASES. 

the nerve-substance is soft and can be washed away with a 
stream of water. The red color tends to disappear when the 
condition has existed for any length of time ; " white soften- 
ing " rather than " red softening " is then said to exist. The 
color is, indeed, from the beginning not an essential point, de- 
pending merely on the amount of blood in the tissues. In such 
softened patches, when the detritus is examined microscopi- 
cally, may be seen remains of nerve-elements, particularly of 
white fibres, in which the myeline is breaking up; swollen 
and indistinct axis cylinders and nerve-cells; large corpuscles 
containing fatty granules, which doubtless come from the 
degenerating nerve-fibres. 

Acute inflammation with softening may occur in the brain 
or cord; acute inflammation of a nerve-trunk affects the con- 
nective tissue primarily in most instances; but in the small 
nerve-branches acute parenchymatous disease occurs, concern- 
ing which we can hardly say whether it should be called in- 
flammatory or degenerative. 

Abscess of Brain. — A further result of inflammation, in 
the brain at any rate, is abscess. Such abscesses may occur 
in various parts of the brain ; perhaps the commonest seats 
are the cerebellum and the temporo-sphenoidal lobes. The 
principal conditions that lead up to intra-cranial abscess are 
— injuries to the head, disease of the cranial bones, especially 
of the petrous bone in connection with old middle-ear disease, 
otorrhcea, accumulations of pus in the pleura, or in dilated 
bronchi, pyaemia. Such an abscess may attain to a consider- 
able size, and last a long time without giving rise to definite 
symptoms. When of long standing it has a distinct wall, 
which separates it from comparatively healthy brain ; in more 
recent or progressive cases the sides are ragged and formed of 
diffusely softened brain tissue. The contents are often very 
foul. Such abscesses may prove fatal by setting up acute 
inflammation and softening in their neighborhood, or by 
perforation into the ventricles, or into the meninges, setting 
up an acute meningitis. 



MORBID ANATOMY OF NERVOUS SYSTEM. JJ 

In chronic inflammation of the nerve-centres, the results 
of the process are chiefly evidenced by changes in the inter- 
stitial tissue. The neuroglia becomes thickened, and its nuclei 
increased in number. The small vessels are enlarged and 
multiplied. The nervous elements are broken up as in acute 
inflammation, but there is more time for the removal of their 
products; hence little may be seen of them, save spaces left 
empty in the thickened neuroglia, or filled with broken-up 
myeline. The result of the interstitial overgrowth is to pro- 
duce a condensation, rather than softening, of the tissues, to 
which the term "sclerosis " is sometimes applied. A similar 
result is produced when there has been a slow destruction of 
the nerve-elements from other causes ; thus, when there has 
been a primary degeneration of these elements, interstitial 
overgrowth follows, so that before long it is impossible to de- 
termine microscopically whether the disease originated in the 
parenchyma or the interstitial tissue. 

Degeneration. — We will next consider this process of 
degeneration, which is one of great importance in nervous 
pathology. 

The simplest instance of degeneration is that which occurs 
in a motor nerve-trunk after section. This has been called 
" Wallerian degeneration" of nerve-trunks, after Augustus 
Waller, the physiologist who first described it. The motor 
fibres of the nerve-trunks issue, as we have seen, from the 
large cells of the anterior gray horns of the spinal cord. One 
function of these cells is to maintain the nutrition of the 
fibres, and of the muscles to which they are distributed. 
Hence, when this trophic influence is removed, either by the 
experimental process of cutting the nerve, or pathologically 
by destruction of the cells (acute anterior polio-myelitis), or 
destruction of the nerve-trunk (acute neuritis or injury from 
without), degenerative changes set in as follows: — 

The axis cylinders, according to most authorities, degene- 
rate and disappear. 
7 



78 NERVOUS DISEASES. 

The medullary substance breaks up, first into blocks, then 
into rounded masses of various sizes; then it undergoes 
gradual absorption. 

Meanwhile, the nuclei within the sheath of Schwann multi- 
ply and enlarge, their protoplasm increasing apparently at 
the expense of the disappearing myeline. 

The final result of the process is the disappearance of all 
the proper nerve-elements, leaving only an empty and shriv- 
eled sheath of Schwann. 

Changes also go on in the muscles, the terminal nerve- 
organs (end-plates) atrophy ; the nuclei of the muscle fibres 
multiply, while the contractile substance loses its striation ; 
the interstitial substance increases, and eventually, if the pro- 
cess continues unchecked, replaces the muscle tissue. 

The conditions which produce this degeneration are destruc- 
tion of the trophic cells, or a break in the axis cylinders 
which connect them with the parts below. 

Secondary Degeneration in Nerve-centres. — An- 
alogous changes take place in the fibres of the central nervous 
system. Taking first the best known set of fibres — viz., the 
motor — we observe that at their origin in the cortex cerebri 
are placed large nerve-cells, which have the same relation to 
them as have the anterior cornual cells to the motor fibres of 
the peripheral nerves. If these cells are destroyed by disease 
of the cerebral cortex, or their connection with the fibres 
below severed, as by cerebral hemorrhage or softening, in- 
volving the internal capsule, or by transverse lesion of the 
cord, then degeneration commences in the fibres below the 
lesion. The process consists in changes in the axis cylinders, 
which first enlarge, then break up ; breaking up of the mye- 
line into a granular detritus, then fusion of the diseased axis 
cylinders and myeline sheaths ; subsequently, the neuroglia 
increases, and at length replaces the nerve-elements (scle- 
rosis). These changes are analogous to, but not identical 
with, the Wallerian degeneration of the nerves, the difference 



MORBID ANATOMY OF NERVOUS SYSTEM. 79 

being that (1) in the nerve-trunks there is an active (? inflam- 
matory) process — viz., the multiplication of the nuclei of the 
sheath of Schwann, while in the cord this sheath is wanting ; 
(2) in the cord the earliest changes are in the axis cylinder, 
whereas in the nerve-trunks the condition of the axis cylinder 
is a little uncertain ; (3) that in the nerve-trunks regeneration 
may take place, whereas in the cord this has never been 
demonstrated. The length of fibre affected by this degenera- 



Cervical enlargement. 



-Upper dorsal region. 



■Mid-dorsal region. 




■Lumbar region. 



Secondary Descending Degeneration of Pyramidal Tract (Crossed and 
Direct) from a Case of Cerebral Tumor. 



tion in the cord extends from the level of the lesion to that 
of the cells of the anterior gray horns, and here it stops. 

The same thing may take place in afferent nerve-fibres. 
For instance, suppose the tract known as the posterior median 
column is cut off from its cells of origin, which are probably 
situated in the ganglia of the posterior nerve-roots, either by 
disease of these nerve-roots or by a transverse lesion of the 
cord, degeneration of the tract sets in, extending upward 
from the lesion to the cells of the post-pyramidal nuclei in 



80 NERVOUS DISEASES. 

which the tract terminates. Similar degeneration occurs in 
the fibres of the cerebellar tract, and of the antero-lateral 
tract under appropriate conditions. Such degeneration is 
called "ascending" when it occurs in afferent fibres, 

Fig. 32. 
a. Upper cervical region. 



b. Cervical enlargement. 



c. Upper dorsal region. 



d. Lower dorsal region. 



e. Lumbar enlargement. 

Secondary Ascending Degeneration of the Postero-Median Columns. 
From a case of tumor involving the Cauda equina and lower part of the cord. In E the 
postero-lateral columns are involved ; above this only the postero-median. The 
cerebellar and antero-lateral tracts are healthy. 

"descending" when in efferent fibres, from the direction, 
up or down the cord, in which it is propagated. 

The process in all these cases is known as " secondary 
degeneration," and it is governed by the following laws : — 

1. That fibres degenerate when separated from their cells 
of origin, or when those cells are destroyed. 



MORBID ANATOMY OF NERVOUS SYSTEM. 8 1 

2. That the degeneration reaches in the direction in which 
the fibres normally conduct, toward centre or periphery, as 

Fig. 33. 



. Upper cervical 
region. 






. Cervi, 

region. 



D. Lower dorsal re- 
gion. 



. Upper part of 
lumbar enlarge- 
ment. 



F. Lower part of 
lumbar enlarge- 
ment. 

Secondary Degeneration, after Transverse Myelitis of 3D Dorsal 
Segment of Cord. 
a, b, and c the degeneration is ascending, and occupies the postero-median columns, 
the direct cerebellar, and antero-lateral tracts. In d, e, and F, the degeneration 
is descending, and occupies the crossed pyramidal tracts. 



the case maybe — i.e., there is no degeneration of afferent 
fibres below a lesion, nor of efferent above it. So invariable 
has this rule been found, that conversely the function, afferent 



82 NERVOUS DISEASES. 

or efferent, of a nerve-tract may be inferred from the direction 
in which its fibres degenerate. 

3. That the degeneration stops short at the nerve-cells in 
which the fibres terminate. 

This limitation of the disease to definite nerve-tracts, and 
the definite direction taken by it in the line of their normal 
conduction, seem to show that its primary seat is in the nerve- 
elements and not in the interstitial tissue. Yet, as has been 
said, the perishing of the nerves appears to involve overgrowth 
of the neuroglia, so that when the process has existed for any 
time it may be absolutely indistinguishable, so far as micro- 
scopic appearances go, from chronic inflammatory disease 
affecting the neuroglia primarily. '''Sclerosis" is the result 
in either case. 

Primary Degeneration in Nerve-Centres. — In addi- 
tion to this "secondary " process of degeneration, caused by 
disease or injury which separates the fibres from their trophic 
centre, it appears that degeneration may arise independently 
of such lesion. It is then called " primary." Such primary 
degeneration may be "systematic " or "diffuse." It is (a) 
systematic when one or more definite nerve-tracts are picked 
out by the disease, much as in secondary degeneration. Thus 
the tracts of the posterior columns degenerate in ordinary 
tabes, and the pyramidal tracts in amyotrophic lateral sclerosis ; 
sometimes they both degenerate together. The more strictly 
"systematic" such disease is, the greater is the probability 
that it is primarily nervous and not interstitial. But on this 
point some uncertainty may prevail — first, because such pri- 
mary degeneration does not limit itself to known nerve-tracts 
with such accuracy as does the secondary form ; secondly, 
because our knowledge of its minute anatomy in the early 
stage is imperfect, and that of the later stages, as pointed out 
above, does not help us. 

(/S) Diffuse degeneration is unselective, irregularly situ- 
ated, and spreads along no definite lines. The typical example 



MORBID ANATOMY OF NERVOUS SYSTEM. 83 

of this is the disease known as insular or disseminated sclerosis, 
in which patches of degeneration are found, irregular in shape 
and situation, and affecting any part of the nervous centres or 
even the peripheral nerves. They exhibit the microscopic 
characters of interstitial overgrowth with nerve disintegration. 
Another example of diffuse degeneration is, a widely spread 
induration and atrophy which occurs principally in the cortex 
cerebri in young children, who are the subjects of hereditary 
syphilis. In such examples it is difficult to say how much 
may be due to chronic inflammation, and how much to primary 
nervous degeneration. 

So far we have chiefly spoken of degeneration of the white 
matter, wherein it can best be studied. Degeneration may 
affect the nerve-cells also. Thus, in the " spinal " forms of pro- 
gressive muscular atrophy there is found a degeneration of the 
anterior cornual cells. This is often associated with similar 
disease in the white matter of the pyramidal tracts. Acute 
disease of the same cells occurs in infantile spinal paralysis, 
but this is most probably inflammatory. 

The causes of nervous degeneration, other than secondary 
degeneration, are very obscure. Probably they must be 
sought among some such influences as these — antecedent con- 
stitutional diseases, such as syphilis, and perhaps other specific 
diseases; toxic influences — e.g., lead, alcohol, ergotism, etc. ; 
inherited or congenital vulnerability of the nervous structures 
which are affected ; over-use, or actual injury. 

Disease Originating Outside the Nervous Paren- 
chyma — (a) Vascular Disease. — Many diseases of the 
nervous system depend, as already said, on causes extrinsic to 
the nervous substance. A large proportion of these arise in 
the vessels. 

Cerebral Hemorrhage. — Hemorrhage is common in 
the cerebral hemispheres. It usually originates from a point 
just outside the lenticular nucleus — i.e., from one of the exter- 
nal divisions of the central branches of the middle cerebral 



»4 NERVOUS DISEASES. 

artery {vide p. 71). The size of such a hemorrhage may 
vary greatly. As it increases it presses upon the basic ganglia 
and internal capsule from without inward, plows up the 
tissues composing them, and finally may rupture into the 
lateral ventricle, flooding with blood this ventricle, and per- 
haps also the third and opposite lateral ventricle, and even 
penetrating through the Sylvian aqueduct to the fourth ven- 
tricle. A large hemorrhage of this description may find its 
way out at the descending cornu of the lateral ventricle, or 
break through the floor of the third ventricle, and so fill with 
blood the sub-arachnoid space at the base of the brain. Such 
a large hemorrhage is necessarily fatal ; smaller hemorrhages 
in course of time become encysted and gradually dry up, and 
may eventually leave only a yellowish scar. Hemorrhages 
originate either from rupture of an atheromatous artery, a 
condition in association with which we commonly find granu- 
lar kidneys and cardiac hypertrophy, or from small aneurisms, 
or from vessels which have undergone fatty degeneration. 
Aneurisms are found not only in the central arteries, in which 
position they are usually small and multiple, and are known 
as miliary aneurism, but also upon the arteries of the circle 
of Willis or of the meninges, where they are more frequently 
of larger size and single. Again, cerebral hemorrhage may 
occur in a vascular new growth, and such a growth should 
always be looked for when the hemorrhage is in an unusual 
situation, as, for instance, the sub-cortical white matter. 
Hemorrhage in the pons is not uncommon ; in the spinal 
cord, apart from injury or new growth, it is rare. 

Plugging of Cerebral Vessels. — Plugging of the cere- 
bral arteries may be due either to embolism or thrombosis. 
In either case, if there be complete obstruction, and if the 
artery affected, as is the case with the central arteries, have 
no anastomoses, the result is softening of the district supplied 
by it, a necrosis and disintegration of the nerve-tissue, with 



MORBID ANATOMY OF NERVOUS SYSTEM. 85 

corresponding abolition of function. From Embolism. — 
In embolism this plugging is sudden, and is due to the impac- 
tion by the blood-stream of some foreign body, most fre- 
quently a fragment of blood-clot or a cardiac vegetation. 
Thus cerebral embolism is often a sequela of valvular disease. 
Sudden cerebral symptoms in the course of such valvular dis- 
ease may, however, be due to hemorrhage, for a previous 
embolism may have caused weakening of the vascular wall, 
resulting in aneurism. The middle cerebral artery is usually 
the seat of embolism, and that of the left side, it is said, more 
frequently than the right. 

From Thrombosis. — Thrombosis of an artery follows 
as a secondary process upon embolism, sealing and complet- 
ing the obstruction ; or originates from disease of the arterial 
wall, such as the roughening of atheroma, or the partial occlu- 
sion which results from syphilitic deposit. The process is 
gradual, though the actual nervous symptoms may be sudden, 
and it may have a tendency to spread. Thrombosis of the 
veins and sinuses results in deep punctate congestion, with 
softening of the district whence the veins are derived. It 
may occur in the proximity of diseased bone, or in such consti- 
tutional states as the cancerous cachexia, gout, anaemia, the 
puerperal condition. 

Vascular Disease as a Source of Spinal Softening or 
Spinal Sclerosis. — In the spinal cord softening is common, 
just as hemorrhage is rare. It may be impossible to say 
whether it is the result of previous inflammation or of de- 
ficient blood-supply. Softening of the lower parts of the 
cord has been explained, on the latter supposition, by the 
lengthy course taken by the vessels of this district along the 
elongated nerve-roots. Again, a form of spinal sclerosis has 
been described by some authors in connection with vascular 
disease. It is said to spread from diseased arteries as a focus, 
and thus to be distributed longitudinally in the cord, so as to 



86 .NERVOUS DISEASES. 

simulate in a measure the " systematic " scleroses which we 
have described above. 

(/3) Disease of Nerve Envelops — (i) Bones. — Dis- 
ease of their envelops — viz., the bones and meninges — se- 
riously affects the nerve-centres themselves. Caries of the 
vertebrae, usually associated with angular curvature (Pott's 
disease), sets up an inflammatory thickening of the mem- 
branes beneath, and this in its turn injures the cord itself, 
partly by compression, partly by spread of inflammation to 
its substance. This has been called compression myelitis, 
Disease of the cranial bones — necrosis, caries, or syphilitic — 
may cause thrombosis of the adjacent sinuses, meningitis, or 
an intra-cranial abscess. Chronic purulent catarrh of the 
middle ear, with disease of the petrous bone, often has one 
of these results. 

(2) Meninges. — Primary affections of the dura mater are 
not very common. Hsematoma of the dura mater occurs 
chiefly in the cerebral dura, and presents the appearance of a 
flat cake upon the inner surface of the membrane, having the 
general appearance of blood-clot.. Whether it is simply blood- 
clot more or less encapsuled and organized, or whether it is 
the result of an inflammatory exudation into the meshes of 
which blood has been extravasated, is still uncertain. In the 
spinal cord, particularly in the cervical region, the dura mater 
is liable to a form of chronic inflammation which causes much 
thickening of its inner surface ; this has been called hyper- 
trophic pachymeningitis. Chronic affections of the cerebral 
dura are most common among the inebriate, the syphilitic, 
and the insane. 

Affections of Pia and Arachnoid. — Disease of the inner 
membranes, pia and arachnoid, is more important, both be- 
cause of their greater proximity to the nerve-substance, and 
because the pia carries the nutrient vessels. In the brains of 
alcoholic subjects a diffuse milky thickening of the arachnoid 



MORBID ANATOMY OF NERVOUS SYSTEM. 87 

is found, with excess of sub-arachnoid fluid, and shrunken, hard 
convolutions beneath. In children a chronic or subacute 
meningitis may arise, limited to the parts around the occipital 
foramen. Syphilitic meningitis is subacute. It occurs in 
the brain in the form of patches, over which the membrane is 
thickened and infiltrated with thick, yellowish lymph ; the 
inflammation may spread to the cortical substance beneath. 
A similar process may occur in the cord ; here it may extend 
over a very considerable length of membrane, affecting also 
the superficial layers of the cord (meningo-myelitis), and the 
nerve-roots as they pass outward. Acute meningitis is 
often secondary to disease of the adjacent structures, the 
scalp, bones, dura mater,- or sinuses. -A .-very frequent cause 
is ear-disease, with disease of the petrous bone. Disease of 
the nasal cavities and of the ethmoid bone may have a sim- 
ilar result. Acute specific diseases form another cause for 
meningitis. Under this head come pyaemia, cerebro-spinal 
meningitis, tuberculosis, and perhaps other acute diseases. 
Pyasmic meningitis is suppurative, and may be spread over 
the whole cerebral surface. ■ Tubercular meningitis has 
limitations as to its seat, and may show other character- 
istic appearances. Thus, as a rule, it is limited to, or at least 
most marked in, the following places: the base of the brain, 
the fissures of Sylvius, the upper surface of the cerebellum. 
Tubercular meningitis of the convexity only is decidedly 
uncommon. There is more thickening and less purulent 
effusion than in the other acute forms of meningitis ; and the 
effusion consists of scanty, sticky lymph held in the interstices 
of the membrane rather than of actual pus. Gray tubercles 
can often be seen studded along the vessels of the meninges, 
particularly in the Sylvian fissures. These, however, may be 
so minute as scarcely to be recognized by the naked eye ; in 
that case the diagnosis must be made by the microscopic 
examination of the membranes, the localization of the men- 
ingitis, and the existence of tubercle, or caseous matter in 



88 NERVOUS DISEASES. 

other organs. For tubercular meningitis is usually part of a 
general tuberculosis. The brain substance in the neighbor- 
hood of the meningitis is frequently reddened and softened ; 
the choroid plexus may share in the inflammation of the men- 
inges ; where there is a large effusion of fluid into the ven- 
tricles, these become greatly distended, and on the surface of 
the hemispheres the sulci become obliterated, the convolutions 
flattened, the cortex bloodless from pressure of the effusion, 
while the brain-substance in the neighborhood of the ven- 
tricles becomes quite soft and macerated. In some instances, 
perhaps more frequently than is usually thought, tubercular 
meningitis affects the cord as well as the brain. In the acute 
specific . disease known as cerebro-spinal meningitis this is 
the rule. 

Lastly, it must be remembered, for it is important clini- 
cally, that disease of the bones and meninges affects not 
merely the nerve-centres, but also the nerve-trunks and nerve- 
roots of the neighborhood. Thus syphilitic disease at the 
base of the skull causes varied paralyses of the cranial nerves ; 
caries of the petrous bone causes facial paralysis ; disease ot 
the spinal column and meninges causes symptoms of pain and 
paralysis referable to the adjacent spinal nerve-roots. 

(y) Tumors. — Tumors are a frequent source of nervous 
disease. Under this head we may enumerate — 

I. Such foreign bodies as hydatids, which may be found in 
the brain or, still more rarely, in the spinal cord ; simple 
cysts, of unknown origin, which appear to be not uncommon 
in the cerebellum. 

II. Inflammatory new growths, which form the local mani- 
festation of a specific disease. Under this head come the 
nodular thickenings or fusiform swellings of the nerve-trunks 
found in leprosy. Syphilis also may produce not only men- 
ingeal and arterial disease, as indicated above, but also an 
infiltration or thickening of nerve-trunks, or, still more com- 
monly, distinct gummatous tumors. These latter may occur 



MORBID ANATOMY OF NERVOUS SYSTEM. 89 

either in the brain or spinal cord ; they are said usually to be 
so placed as to manifest some connection with the pia mater 
or the choroid plexus. Hence, the cortex cerebri is a not 
unusual site for them. Since the role of syphilis in the pro- 
duction of nervous disease has been recognized, and anti- 
syphilitic remedies used almost as a matter of routine, gum- 
mata have been less frequently seen post-mortem. Tubercular 
disease may present itself in the form of caseous masses, 
deeply situated in the nervous centres. These are perhaps 
most frequent in the cerebellum and its neighborhood. They 
may be single or multiple, may run to a considerable size, and 
may exist for a length of time. 

III. Tumors in the stricter sense — i. e., new growths of 
definite microscopic type, and with tendency to increase. 
These are mainly carcinomata and sarcomata. Carcinomata 
are perhaps the least common of the two, and when found in 
the nerve-substance are secondary to growths elsewhere. But 
they may also spring from the dura mater or the bones. Of 
sarcomata, a common sort is that known as glioma, a small 
round-celled growth which originates in the neuroglia. It 
may affect any part of the nervous centres. In glioma of the 
pons Varolii the whole of this organ may be enlarged, 
unequally perhaps, and with lobulation and some distortion 
of its surface, but still preserving its general shape. On sec- 
tion, the whole pons is found to be diffusely infiltrated with 
new growth. Other forms of sarcomata — large-celled, spindle- 
celled, or with cells of mixed type, myxo-sarcomata, cystic 
sarcomata — are also found. They may be primary or sec- 
ondary; single, multiple, or even symmetrical; and may 
affect almost any part of the nervous system or its envelops. 
Among the more curious sites may be mentioned the nerve- 
trunks at the base of the brain ; a spinal nerve-root ; the 
spinal meninges, enwrapping the cord for a considerable dis- 
tance; the dura mater in several of the cerebral fossae simul- 
taneously. The nerve-substance of the cerebral hemispheres 



9 o 



NERVOUS DISEASES. 



is perhaps their commonest seat. And here it may be 
remarked (i) that a new growth may be almost indistin- 
guishable by the naked eye from softish cerebral tissue ; (2) 
that cerebral new growths are often very vascular, and their 
vessels may suddenly give way, and hence both the clinical 
symptoms and the post-mortem appearances may simulate to 
a certain extent those of simple cerebral hemorrhage. 



CHAPTER III. 

ON CERTAIN GENERAL SYMPTOMS AND 
METHODS OF INVESTIGATION. 

Before describing the several varieties of nervous disease, 
it may be well to consider certain symptoms which are common 
to many of them. These symptoms may be roughly grouped 
into anomalies of the motor or sensory functions, such anom- 
alies being either on the side of defect (paralysis), excess 
(irritation), or perversion; anomalies of reflex or of co- 
ordinative movements or of the intellectual functions. 

Motor Paralysis in its Relations to Lesions at 
Different Sites. — Loss of the power of voluntary move- 
ment (motor paralysis), and in a less degree loss of the power 
of sensation (sensory paralysis), supplies us with the most 
definite symptoms for purposes of diagnosis, and particularly 
diagnosis of the locality of the disease. A recapitulation of 
the course of the motor and sensory fibres will aid us in 
understanding the forms of motor and sensory paralysis. 

Course of the Motor Tract. — The motor fibres com- 
mence in the ganglion cells of the cerebral cortex. Here (it 
will be remembered) the nervous mechanism for each half of 
the body is separated in its respective hemisphere, and, further, 
the centres for the various parts of the same side — viz., face, 
arm, leg, etc. — are spread over a tolerably wide area. But 
as they descend through the corona radiata the fibres from 
these centres gradually approximate, till they reach the pos- 
terior limb of the internal capsule. Here they lie in close 
juxtaposition, though they are not intermingled. Proceeding 
downward through the crus cerebri they reach the pons, where 
9i 



92 NERVOUS DISEASES. 

they still lie within a small area, though broken up and sepa- 
rated by the transverse fibres which cross between the cere- 
bellar hemispheres. At the level of the pons some of them — 
viz., those for the eyes, face, and tongue — cross, decussating 
with those of the opposite side, and end in the nuclei of their 
respective cranial nerves. The remainder continue their 
course till they reach the junction of the medulla and cord. 
Here they also cross to the opposite side (decussation of the 
pyramids). Thence they pass down in the opposite half of 
the cord, mainly within the posterior part of its lateral 
column — i. e., as the crossed pyramidal tract — (some running 
also without decussation in its anterior column as the direct 
pyramidal tract) till they terminate in the large cells of the 
anterior cornu, and principally at the levels where these cells 
are most abundant — viz., at the cervical and lumbar enlarge- 
ments. Thus, from the cortex cerebri to the motor nuclei of 
the cord and medulla the fibres are uninterrupted by ganglion 
cells. From these spinal nuclei motor fibres start afresh and 
pass outward from the central nervous axis, either as cranial 
motor nerves or anterior spinal nerve- roots. These latter 
soon join the sensory roots, fuse with them into a nerve- 
trunk of mixed sensory and motor function, and thus run till 
they approach their distribution, where filaments are again 
separated out for the supply of the various muscles and 
cutaneous areas. 

Course of the Sensory Tract. — Concerning the course 
of the sensory fibres within the central nervous axis much less 
is known, but this much may at least be said : those which 
come from the one side of the body enter the cord by the 
corresponding posterior nerve-roots, and soon after entering 
it cross to the opposite side of the cord.* Their exact 
position as they run upward in the cord we do not know. 

* Even this statement, in the light of some recent researches, may need 
revision. 



METHODS OF INVESTIGATION. 93 

But at the level of the pons and the crura cerebri the sensory 
fibres probably lie in the tegmentum (viz., the posterior or 
dorsal part of these regions), just as the motor fibres lie in the 
crusta (viz., the anterior or ventral part). Higher still, at 
the level of the internal capsule, the sensory fibres, including 
now those from the organs of special sense, are gathered into 
a bundle which lies behind the bundle of motor fibres, and 
constitutes the posterior third of the posterior limb of the 
internal capsule. Thence they probably diverge, spreading 
through the corona radiata to reach the sensory areas of the 
cerebral cortex. 

From this arrangement of the motor and sensory tracts 
there follow some important facts regarding the distribution 
of paralysis. 

Paraplegia. — When the spinal cord is affected by a trans- 
verse lesion, say in the dorsal region, sensation and motion 
are lost in all the parts below. This is called "paraplegia." 
The bilateral distribution of the symptoms is almost charac- 
teristic of spinal disease. The paraplegia may be complete or 
partial in degree, both as regards motion and sensation ; or 
motion only may be affected, since the two motor tracts lie 
not far apart, and are for some unexplained reason more easily 
affected than the sensory. 

Hemiparaplegia. — If the lesion does not reach right 
across the cord, but across one (lateral) half of it only, then 
motor paralysis results (of the parts below) upon the side of 
the lesion, because the motor tract for one-half the body (say 
the right) runs in the corresponding (right) half of the cord ; 
but there is sensory paralysis of the opposite side, because the 
sensory fibres of one-half the body (say the left) cross after 
entering the cord, and run in its opposite (right) half. This 
condition, a rare one, is called " hemiparaplegia." 

Hemiplegia. — Passing now to the brain, if there is a 
lesion in the neighborhood of one internal capsule (a common 
event), then the motor fibres going to the face, arm, and leg 



94 



NERVOUS DISEASES. 



Fig 34. 



Lesion of cerebral mo- 
noplegia (brachial). 



Lesion of ordinary 
hemiplegia. 



Lesion of cross pa-, 
ralysis (face of same 
side with limbs of 
other side). 



A lesion causing para- 
plegia. 



A lesion causing hemi- 
paraplegia. 



Cortical centre for op- 
posite leg. 



Cortical centre for op- 
posite arm. 



Cortical centre for op- 
posite side of face. 



Internal capsule (pos- 
terior limb). 



Decussation of pyra- 
mids. 




pyramidal 



Crossed pyramidal 
tract. 



Sensory nerves enter- 
cord, and decus- 
sating soon after 
entry. 



Motor nerves to lower 
b. 



Diagram to Show the General Arrangement of the Motor Tract, and the 
Effect of Lesions at Various Points. 



METHODS OF INVESTIGATION. 95 

of the opposite side are likely to be interrupted, and there 
ensues the familiar condition of one-sided paralysis known as 
"hemiplegia." Hemiplegia points to a cerebral lesion as 
does paraplegia to a spinal. According to the part of the 
capsule which is involved, the hemiplegia is motor, sensory, 
or both combined. The abolition of motor function is 
usually the most striking and most permanent symptom. 

A lesion in the pons may be large enough to involve both 
sides of it ; then both arms and both legs will be paralyzed. 
Probably there will also be symptoms referable to some cranial 
nerve ; the commonest of these is contraction of the pupils 
(from irritation of the third nucleus?). Cross-paralysis. 
— A one-sided lesion of the pons produces the characteristic 
symptoms of " cross-paralysis." This depends on the fact that 
a cranial nerve is caught after its decussation, and the motor 
tract of the limbs before its decussation. Thus the nerve 
paralysis is on the side of the lesion, and the limb paralysis, 
as in ordinary hemiplegia, on the opposite side. In disease 
of the upper part of the pons the facial nerve of the same side 
is paralyzed and the limbs of the other side ; in disease of the 
crus cerebri, the third nerve of the same side with the limbs 
of the other. The hemiplegia, if the lesion lies near the pos- 
terior (tegmental) aspect of the pons, may be sensory rather 
than motor. 

Monoplegia. — By "monoplegia" is meant paralysis in- 
volving a single part only — e.g., one limb, one side of the 
face, etc. This may happen under very different conditions. 

A. The lesion may be cerebral, affecting either (i) the 
cortex or sub-cortical white matter of the motor area before 
the motor strands have joined in the internal capsule ; or 
(2) the capsule, but to such a limited extent as to pick out 
one only of its constituent strands, the face, arm, or leg-fibres. 

B. The lesion may be spinal. If it be limited to a moder- 
ate length of the anterior gray cornua of one side, paralysis 
of one limb or one set of muscles in a limb will result. Unlikely 



96 NERVOUS DISEASES. 

as such a limitation might appear a priori, it often occurs 
practically, as in cases of infantile paralysis. 

C. The lesion may be neural, affecting either a nerve-trunk 
or the nerve-endings. Let us defer, for simplicity's sake, the 
consideration of disease of nerve-endings (peripheral neuritis), 
which is indeed more often bilateral than monoplegic, and 
let us consider the points of diagnosis between the other 
forms of monoplegia. 

Cerebral monoplegia (A) differs from that of spinal (B)and 
neural (C) origin in these points mainly : in the two latter 
forms there are disturbances of nutrition in the paralyzed 
muscles, evidenced by wasting, flaccidity, and alteration of 
electrical reactions, owing to interference with the function 
of the anterior cornual cells ; whereas in the cerebral form 
the electrical reactions are normal, wasting, if any, is less 
marked and less early ; and there is a tendency to rigidity. 
In the spinal and neural forms, the paralysis is absolute ; that 
is to say, volitional, reflex, and associated movements are all 
abolished, whereas in cerebral paralysis the leg may move 
when tickled, or the arm when the patient yawns. Tendon 
reactions, too, are abolished in the spinal and neural forms, 
preserved or exaggerated in the cerebral. (There may be also 
differences in the distribution of the paralysis within the limb.) 

Spinal monoplegia (B) due to disease of the anterior 
cornual cells differs from neural (C), due to disease of a nerve- 
trunk, in the following respects. In the former there is no 
anaesthesia ; in the latter, except in disease of a purely motor 
nerve-trunk such as the facial, we should expect anaesthesia. 
In the former, again, the distribution of the paralysis should 
follow the grouping of the spinal segments ; in the latter it 
should follow the anatomical distribution of the .nerve. 
There will remain, however, for both forms the common 
characteristic of muscular wasting or flaccidity, plus electrical 
changes, except in the few instances where the disease is 
either very mild or very recent. 



METHODS OF INVESTIGATION. QJ 

Cerebral monoplegia (A) may arise from a lesion either (i) 
in or near the cortex, or (2) in the internal capsule. The 
former is more common, because at the cortex the motor 
tract is spread over a wider area and its constituent centres 
are more separate than in the region of the internal capsule. 
Small capsular lesions may, it is true, pick out one of the 
several bundles for face, arm, leg, etc. But since such a 
lesion is usually a hemorrhage, the immediate shock of which 
extends beyond its anatomical limits, we should expect a his- 
tory of hemiplegia which in time has narrowed down to 
monoplegia. Cortical lesions, on the other hand, which are 
frequently progressive (tumors, gummata, meningitis, and the 
like), begin with monoplegia, which may spread into a hemi- 
plegia. 

Examination of Motor Paralysis. — Motor paralysis, 
if of any degree, is a symptom sufficiently obvious both to 
the physician and the patient. It may be necessary, however, 
to distinguish it from weakness consequent on mere exhaus- 
tion, such as occurs after acute diseases, from inability to 
move caused by pain on movement, or by joint disease, or 
(in children) by separation of an epiphysis. A hemiplegia, 
when the patient is in a state of coma, may sometimes be 
made out by the flaccid way in which the limbs of the par- 
alyzed side drop when we raise them, and then allow them to 
fall ; by the distortion of the face toward the non-paralyzed 
side, or by the puffing out of the cheek upon the sound side. 

Paralysis of a minor degree is often called " paresis." The 
effect of such minor paralysis upon the finer movements of the 
hands may be confused with the awkwardness produced by 
loss of sensory or of co-ordinative power. Incomplete loss of 
power in the leg is shown by the patient dragging the limb as 
he walks ; the toes of the boot may sometimes be noticed to 
be worn down thus. An instrument called a dynamometer 
is sometimes used for estimating the amount of power retained 
by the hands (strictly speaking, by the flexors of the fingers 



98 NERVOUS DISEASES. 

and thumb). It is an oval spring, which the patient is made 
to squeeze; the resistance which he thus overcomes is recorded 
by a dial and index fixed in the centre of the spring. It is 
useful for estimating the relative strength of the two hands ; 
but since there is a certain knack in squeezing it far, it is less 
trustworthy for absolute measurements. 

Loss of power in individual muscles is detected in some of 
the following ways. Knowing the normal action of the 
muscle, we tell the patient either to fix the limb in such a 
position or bring it into such a position as involves the 
contraction of the muscle, while we ourselves apply a counter- 
force. Thus, for the biceps cubiti we bid him keep the elbow 
semiflexed while we try to straighten it out ; for the ilio-psoas 
we bid him while sitting to bring the thigh toward the body 
while we apply pressure downward on the knee. Or we may 
guess the nature of the paralysis from the position produced 
by the unbalanced action of antagonistic muscles, witness the 
claw-hand in paralysis of the interossei, or from the expedients 
the patient adopts in performing certain movements, witness 
the way in which a child with weakness of the erector spinge 
climbs up on his knees in the endeavor to get up from the 
ground. 

Examination of Sensory Paralysis. — Sensory pa- 
ralysis, commonly called anaesthesia, is more complicated in its 
nature and more difficult to test than motor. We must 
distinguish various modes of sensation. 

(1) Tactile sense — i.e., the feeling experienced when the 
skin is touched. This may be tested by light touches with the 
feather of a quill-pen, or by touching the hairs of the part 
examined. The eyes should be securely closed, the surface 
tested should not be cold, the fingers, etc., should not be 
moved. Lastly, allowance must be made for the patient 
getting puzzled and for impatience on his part (or on the 
part of the operator). In certain cases the patient may feel 
the touch but cannot say where it is, or localizes it in the 



METHODS OF INVESTIGATION. 99 

wrong place. In rare cases the patient will refer the touch to 
the corresponding part of the opposite side of the body ; this 
has been called " allochiria." It is frequent to hear com- 
plaints of numbness, deadness, and the like, pointing, no 
doubt, to minor degrees of anaesthesia, and yet to be unable 
to detect anything by examination. 

(2) Sense of temperature. This may be tested with hot 
and cold spoons or sponges ; or by test-tubes filled with water 
of different temperatures; or by alternately blowing and 
breathing on the part. The patient may be unable to 
discriminate between the sensations, or may take the one 
sensation for the other. Sometimes he will start away from 
the application of a cold surface and declare it burnt him. 

(3) Sense of pain. This may be tested by pinching, 
pricking with a needle or pen point, or by the faradic current 
applied with a wire brush. The touch of the object may be 
felt sometimes, but not the pain (analgesia) ; or, again, the 
pain may not be felt till after a distinct interval, owing to 
delay in transmission of the pain-sense. 

(4) Muscular sense. This expression apparently means the 
appreciation we form of muscular tension, whether such tension 
be active, as when we contract our muscles against resistance, 
or passive, as when the limbs are placed in varying positions. 
The muscular sense may be tested in the following ways: — 

(a) By noting the patient's power to discriminate differ- 
ences in weight. This may be done by making him hold in 
his hand balls of similar external appearance, but differing in 
weight. 

(,5; By making him shut his eyes and tell when his limbs 
are put by us into different postures. In this latter test, at 
any rate, the impressions derived from the muscles are supple- 
mented by those from the joints, fasciae, tendons, etc. 

"Muscular sensibility" is sometimes distinguished from 
" muscular sense," as meaning the conveyance from the 
muscles of ordinary tactile impressions when they are handled, 



100 NERVOUS DISEASES. 

or of painful impressions when they are pinched, cut, or 
severely faradized. 

The various modes of sense that we have enumerated may 
be affected separately or together. It seems probable that 
different impressions may be conveyed by different routes 
within the cord, but we do not certainly know the route of 
any one of them. 

Distribution of Anaesthesia. — From the distribution of 
anaesthesia, just as from the distribution of motor paralysis, 
certain inferences may be drawn as to what part of the 
nervous system is involved. In disease of the nerve-endings 
(multiple peripheral neuritis) the anaesthesia involves the 
extremities of the limbs, like a glove or stocking, irrespective 
of the distribution of the main-nerve trunks ; in disease of a 
nerve-trunk the sensory, like the motor palsy, follows the 
distribution of the particular nerve-trunk. In disease of the 
nerve-roots, or of the cord itself, the value of the sensory 
symptoms depends a good deal on the level of the lesion in 
the cord. Thus, in a transverse dorsal myelitis, owing to the 
simplicity of the cutaneous distribution of the dorsal nerves, 
the level reached by the anaesthesia enables us to infer with 
considerable accuracy the segment of the cord which is 
affected. But in a myelitis affecting the cervical enlargement, 
or the lumbar or sacral region, the distribution of the anaes- 
thesia in the limbs is less easily understood. We shall refer 
the reader to the statements already given as to the functions 
of these parts. The import of sensory and motor palsy, when 
they involve opposite sides of the body, spinal hemipara- 
plegia, has been sufficiently pointed out. Anaesthesia de- 
pending upon lesion of the sensory (extreme posterior) part of 
the internal capsule involves the whole of the opposite side of 
the body, face, trunk, limbs, and special senses. Anaesthesia 
from disease of the cortex is a subject incompletely known ; 
but it would appear that the loss of sensation from this cause 
affects the limbs, segment by segment, involving the hand up 



METHODS OF INVESTIGATION. IOI 

to the wrist, the forearm to the elbow, the arm up to the 
shoulder, etc., so that oddly enough the distribution of it 
may resemble that of the anaesthesia from disease of the 
nerve-endings. 

There is this much, however, to be said about sensory as 
compared with motor paralysis, that (except in cases when a 
sensory tract rather than a motor is definitely singled out by 
disease) sensory paralysis is the less marked and the more 
transitory symptom of the two, whether the lesion lie in the 
brain, cord, or nerves. 

Other Anomalies of Motor Function. — The functions 
of motion and sensation instead of manifesting deficiency 
(paralysis) may be morbidly exalted or perverted. 

Convulsions. — Of such motor exaggerations there are 
several important kinds. The convulsions of true epilepsy 
consist of sudden, widespread, purposeless, muscular spasms, 
usually tonic at first (i.e., the muscular contraction is con- 
tinuous), and then clonic (i.e., the affected muscles, relaxing 
and contracting alternately, produce a vibratile movement of 
the affected parts). In the convulsions called epileptiform, 
the movements begin in a definite member and involve the 
rest of the body gradually. These latter attacks are of special 
interest, since it has been shown that they are caused by local 
disease in the motor area of the cerebral cortex ; that the 
principal focus of disease is in the cortical centre for the 
member first attacked by spasm ; and that the spread of the 
convulsions corresponds to the spread of irritation over suc- 
cessively adjacent motor centres. Thus, suppose a convul- 
sion begins in the great toe, it is likely to spread thence up 
the leg and thigh, to the upper limb, and face, because the 
irritation will involve successively the leg, arm, and face 
centres. 

Chorea. — The movements of chorea consist of restless, 
sudden twitches, which vary from mere starts to wild jactita- 
tion of the limbs. They are not paroxysmal, like epileptic 
9 



102 NERVOUS DISEASES. 

convulsions, and the movements themselves are more varied 
and intermittent. They are not rhythmical, like the tremors 
we shall presently notice ; they occur both while the patient 
is at rest, and as an interruption to his voluntary movements. 
From the facts that the twitchings and grimacings of chorea 
resemble sudden voluntary movements, and that they may 
be limited to one side of the body, we may surmise that their 
source is the cerebral hemispheres. 

Athetosis. — In the late stages of hemiplegia, particularly 
when this is incomplete in degree and has originated in child- 
hood, certain slow, continuous movements of the affected 
limbs may be observed, chiefly hyper-extension and wavy 
movements of the fingers, with, perhaps, drawing movements 
of the arm. Such a condition, aptly described by Gowers 
as a " mobile spasm," is called athetosis. 

Tremors. — Several varieties of movement are classed 
under the term " tremors," meaning by this a more or less 
rhythmical shaking. The first consists of such as are seen in 
disseminated sclerosis. Here the limbs are still when at rest, 
but on attempting to use them irregular movements set in. In 
a well-marked case these movements are wide and irregular in 
extent, and they involve the whole hand or arm. To these it 
is usual to oppose a second class — the tremors of paralysis 
agitans. The movements in this disease, at least at an early 
stage, are most noticeable when the limb is at rest, and are 
checked by voluntary movement. They are smaller in extent 
(finer tremors, that is), and affect primarily the small mus- 
cles — viz., those of the thumb and fingers — and are more 
truly rhythmical both in time and in extent. There are many 
other diseases in which tremors occur, and in which the char- 
acteristics to which we have alluded should be noted ; that is, 
whether they are most marked during rest or during effort; 
whether they are fine or coarse movements, rapid or slow, 
rhythmical or irregular. Such diseases are senility, general 
paralysis, hysteria, Graves' disease, mercurialism, alcoholism. 



METHODS OF INVESTIGATION. IO3 

Fibrillary Twitchings. — Another variety of muscular 
over-action may be seen in cases of progressive disease of the 
anterior cornual cells of the cord. Small bundles of the 
muscles which are undergoing atrophy twitch from time to 
time, so as to raise the skin above them, and sometimes even 
so much as to cause a start of their tendon. This is called 
fibrillary tremor, or (where larger parts are involved) fascicu- 
lar tremor of the muscle. 

Spasm, either continuous or intermittent, may sometimes 
be distinctly limited to the distribution of the nerves, as in 
the wryneck produced by contraction of the sterno-mastoid 
and trapezius, or in motor " tic" affecting the facial muscles. 
Or, again, individual muscles, or sets of muscles, may be 
affected. 

Another very common and very important form of muscular 
over-action is the rigidity which accompanies certain chronic 
stages of paralysis. This we shall defer till we speak of tendon 
reactions. 

Anomalies of Sensory Function — Pain. — Exaggera- 
tions and perversions of the sensory functions furnish less 
definite indications of disease than do those of the motor. 
The commonest, pain, is obviously of too wide import to be 
a direct index of nervous disease. But there may be such 
characters about a pain as indicate that the nervous system 
is specially involved. It may be limited to the district sup- 
plied by a particular nerve, as in neuralgia, or it may have a 
peculiar lancinating character, as the "lightning pains" of 
tabes dorsalis, or it may be remarkably paroxysmal. The 
name " causalgia " has been given to a peculiar burning pain, 
which occurs in partially anaesthetic limbs, particularly where 
there has been injury or disease of a nerve-trunk. Tender- 
ness to touch may also be limited to a nerve-trunk, or to 
certain points in its distribution. Thus, in trigeminal neu- 
ralgia tender points may be found where the nerve makes its 
exit from the bones upon the face ; and in nervous women 



104 NERVOUS DISEASES. 

tender points are found over the intercostal nerves, under the 
mammae, in a line with the angle of the scapula, over the 
vertebrae, etc. Particularly well marked, in this latter class 
of case, is the tenderness to pressure in the inguinal regions, 
which has been called "ovarian" tenderness. When tender- 
ness is so marked that merely touching the skin gives rise to 
pain, there is said to be " hyperesthesia," more properly it 
would be called "hyperalgesia." Paresthesia. — Sensa- 
tions described by patients as crawling ("formication"), 
pins and needles, numbness, deadness, and the like, are not 
infrequent, and may indicate, as above noted, a mild degree 
of sensory paralysis. Sensory Aurae. — Lastly, epileptiform 
attacks are sometimes heralded by sensations instead of by 
limited convulsions. These sensory "warnings" are pre- 
sumed to point to a focus of disease in the sensory area of the 
cerebral cortex, and to be thus strictly comparable to the 
motor warnings which we have noticed above. 

Reflex actions form a very important item in the diagno- 
sis of nervous disease. These we may roughly divide into 
three classes ; the organic reflexes, the superficial or skin 
reflexes, and the so-called deep or tendon reflexes. 

The "reflex arc." — The nervous structures concerned 
in a reflex action consist of three main parts : (a) afferent 
fibres which convey the stimulus from the periphery to (/3) 
the centre, consisting of the gray matter of the cord, medulla, 
pons, or cerebrum. In this centre the stimulus is modified 
and rearranged so that it issues as a motor impulse along (j) 
the efferent fibres, which convey it to the muscle or other 
organ which has to be called into activity. If a reflex action 
is present, we may infer that all these parts (together called 
the "reflex arc") are intact. If it is absent, this may be 
due either to disease of the arc itself, or to some perturbing 
influence exercised by some higher part of the nervous centres, 
or to the fact (not unfrequent in skin-reflexes) that the reflex 
is naturally ill-developed, or has become obsolete from dis- 



METHODS OF INVESTIGATION. IO5 

use. The several fragments of the cord with their attached 
nerves constitute a series of reflex arcs ; and each of the reflex 
centres — i. e., each segment of the cord — has a recipient 
(posterior) part and a motor (anterior) corresponding to the 
anterior and posterior nerve-roots.* Disease of any part of 
the arc, central or peripheral, may annul the reflex ; disease 
of the anterior part of the spinal segment, or disease of its 
efferent nerves, causes motor palsy as well as loss of reflex; 
disease of the afferent nerves causes loss of reflex and loss of 
sensation ; but disease of the posterior part of the spinal 
segment may cause loss of reflex without loss of sensation, 
the probable reason being that within the cord the afferent 
fibres take a different course according as they are going to 
the reflex centre or to the sensorium. 

The control exercised by the higher centres over reflex 
actions is a subject of which our knowledge is imperfect ; 
but that such control exists is shown by the facts that reflex 
actions can often be prevented by the will, and that they 
may be exaggerated when cerebral influence has been cut off 
by disease. 

Organic Reflexes. — Let us consider those reflexes which 
have a special bearing on questions of diagnosis, and, first, 
some of the so-called "organic reflexes." The centres for 
micturition and defecation are situated in the lowest parts of 
the cord.f 

Micturition. — The act of micturition is complicated. So 
far as it is purely reflex, its mechanism is this : the urine, 
gradually accumulating in the bladder, supplies, after sufficient 
accumulation, a stimulus to the spinal centre ; the activity of 
the centre thus aroused causes a double action in the bladder 
— viz., contraction of the detrusor urince and relaxation of 
the sphincter, and in this way the bladder is emptied. But, 

*C/p. 21. 

f Probably in the 3d and 4th sacral segments. 



106 NERVOUS DISEASES. 

further, the spinal centre is in communication with the brain ; 
hence the patient is conscious of the stimulus which leads to 
micturition, and can, on the other hand, prevent the act of 
micturition if he chooses. 

Were this prevention or inhibition the only result of the 
influence exercised by the cerebrum, we should expect that 
removal of this influence would simply leave the spinal centre 
free to empty the bladder, unconsciously and involuntarily, 
at stated intervals. But as a matter of fact in cerebral hemor- 
rhages, crushing of the cord above the lumbar region, and 
other injuries and disease which remove the cerebral influence, 
we usually find the bladder distended. Hence it seems that 
the cerebrum acts not only in the way of inhibiting, but also 
of stimulating the micturition centre. If the spinal centre for 
micturition be itself destroyed, distention of the bladder 
results with still greater certainty ; for though the sphincter is 
paralyzed as well as the detrusor, there remains in the urethra 
and parts around it sufficient resistance to the exit of urine to 
cause distention. The bladder rises above the pubes as an 
oval, dull, fluctuating swelling ; urine may dribble from the 
urethra, but this is simply a sort of overflow, which does not 
empty the organ. 

Defecation. — The mechanism of defecation is very simi- 
lar. In health the tonic contraction of the sphincter prevents 
the continuous passage of fasces. During defecation the 
sphincter is relaxed, and the peristaltic action of the bowel, 
reinforced by the contraction of the abdominal muscles, 
expels the faeces. Defecation, like micturition, is not in 
health a purely reflex act ; the spinal centre is obviously under 
the control of the cerebrum, which can inhibit or permit its 
action. We may notice, however, that some of the muscles 
which contribute to the expulsion of faeces, notably the 
diaphragm and abdominal muscles, are innervated from a 
higher level than the sacral cord, in this respect differing from 
the muscles of the bladder. And again, that when the rectal 



METHODS OF INVESTIGATION. IO7 

sphincter is paralyzed by destruction of the sacral centre, there 
is not (as in the case of the urethra) sufficient resistance in 
the soft parts to produce retention. Hence, in such paralysis 
involuntary evacuation of fasces is the rule. 

There exist other lumbar centres whose condition may 
afford us information as to the state of the cord. Thus, by 
destruction of the lumbar cord the act of erection is rendered 
impossible, while in transverse lesions of the cord higher up 
we often find troublesome priapism owing to over-action of 
the centre for erection. 

It need scarcely be added that the organic reflexes, which 
are most essential to life, have their centres in the medulla 
(cardiac, respiratory, gastric reflexes). Affections of these, 
as evidenced (for instance) by continuous vomiting, inability 
to swallow, disturbances of the respiratory or cardiac rhythm, 
are most important in prognosis; they show that disease is 
advancing toward a vital point of the nervous system. 

Superficial or Skin Reflexes. — "Skin" reflexes, or 
superficial reflexes, are the movements which follow when 
certain portions of the skin are tickled or irritated. The prin- 
cipal skin reflexes are as follows : — 

The plantar— tickling the sole causes movement of the toes 
or drawing up of the leg ; the centre is in the upper sacral 
region. The gluteal — irritation of the skin over the glutei 
causes contraction of those muscles ; centre, in lower lumbar 
region. The cremasteric — stroking the skin of the inner part 
of the thigh produces retraction of the testicle on the same 
side; centre, upper lumbar region. The abdominal — stroking 
one side of the abdomen causes contraction of the abdominal 
muscles upon that side ; centre, lower half of dorsal region; 
and stroking the skin over the lower ribs causes a twitch of the 
epigastric region ; this is called the epigastric reflex, centre, 
about mid-dorsal region. The scapular — upon irritating the 
skin between the scapuhe there follows contraction of the 
muscles beneath the skin ; centre, in cervical enlargement. 



108 NERVOUS DISEASES. 

The conjunctival — touching the conjunctiva produces winking ; 
centre, nuclei of fifth and seventh nerves with their fibres of 
connection. 

The pupillary reflexes will be described in connection with 
the eye — vide p. 131. 

Absence of these skin reflexes is not necessarily due to dis- 
ease. They are, indeed, usually present in healthy children, 
but in adults they cannot always be obtained. Some of them 
— e.g., the plantar, cremasteric, abdominal, conjunctival — are 
more constant than others. In cases of unilateral cerebral 
disease, especially at an early stage, it may be found that the 
superficial reflexes on the paralyzed side are absent, or di- 
minished as compared with those on the sound side. In hys- 
terical paraplegia, the plantar reflex may be, so to speak, 
delayed ; that is, we have to tickle the sole a long time before 
the reflex action follows. 

Tendon-Reactions, otherwise called tendon phenomena, 
tendon reflexes, deep reflexes, or "jerks," are more constant 
phenomena in health, and are of extreme importance in the 
diagnosis of disease. Let us first consider the most typical 
example of this class — viz., that which is variously called the 
patellar tendon reflex, the knee-phenomenon, or knee-jerk — 
and which consists in the sudden contraction of the quadri- 
ceps extensor cruris, and (by consequence) sudden extension 
of the knee-joint, which is evoked by a blow upon the ligamen- 
tum patellae, Methods of Examination. — In most cases 
we can obtain it thus : direct the patient to sit with one knee 
comfortably supported across the other, then strike a sharp 
blow (even through the dress) upon the ligamentum patella?. 
This may be done with the finger-tips, with the edge of a 
thin book, or, best of all, with the ear-piece of a stethoscope 
which is shod with a stout india-rubber ring. (These are sold 
by instrument makers for the purpose of percussing the chest.) 
The quadriceps cruris responds by a sharp single contraction, 
which jerks the foot upward. The essential points in the ex- 



METHODS OF INVESTIGATION. IO9 

amination are, that the knee-joint should be partially flexed 
(a position midway between extension and semiflexion is a 
good one), so as to put a certain amount of passive tension 
on the quadriceps ; that the other muscles, particularly the 
hamstrings, should be relaxed, and not consciously or uncon- 
sciously held rigid ; that the blow should be sharp but elastic, 
and should fall accurately on the tendon, not on the bone. 
(Usually a point a little to the inner side of the belly of the 
tendon is the most sensitive.) If no "jerk" of the foot be 
obtained, the knee and thigh must be bared ; we can then 
better localize the blow, and can see or perhaps feel the an- 
swering contraction of the muscle, for this may be present, 
though not strong enough to raise the foot. The patient may 
also be made to sit on the edge of a table with the thighs 
supported as far as the knee-joints, and the legs dangling 
loosely over the side ; or, in children especially, we may 
"stirrup" the foot by taking it in one hand and flexing the 
knee with a light upward pressure. Should the patient be in 
bed, we must remember to flex the knee-joint by lifting it in 
one hand, and we can at the same time feel with this hand 
whether the hamstring muscles are duly relaxed. Should we 
fail after all precautions in obtaining a knee-jerk, we may 
adopt a plan introduced by Jendrassik, sometimes called the 
"arm-tension" method, or method of "reinforcement" — 
viz., tell the patient to hook the fingers of either hand into 
each other and then pull strongly as if to pull them apart, 
while we test the knee-jerk. This distracts his attention, and 
possibly reinforces the contraction by increasing the muscular 
innervation throughout the body. 

Difficulty in eliciting the knee-jerk (in the absence of 
disease) is generally caused as follows: either (1) the patient, 
either from nervousness or from a mistaken idea of helping 
the operator, does not allow the limb to hang flaccidly ; or 
(2) in corpulent people with thick limbs and a short liga- 
mentum patellar, it is difficult to strike the tendon sufficiently 
10 



IIO NERVOUS DISEASES. 

accurately and smartly. In this latter case, a firm blow with 
the edge of the hand may act better than the smart tap with 
the finger-tips or with the india-rubber-shod stethoscope. 

The theory of the knee-phenomenon is still unsettled ; 
some maintain that it is a true reflex action ; others that it is 
a purely muscular contraction, evoked directly by the sudden 
tension put on the muscle by the blow ; others that, though 
the actual contraction is not a reflex act, yet that it requires 
for its development a certain muscular tonus, the maintenance 
whereof is dependent on reflex action. These theories we 
need not discuss, because, clinically speaking, it conforms in 
all the conditions which accompany its presence and absence 
to a true reflex, whatever may be its essential nature physio- 
logically. 

Meaning of Abnormalities in Tendon Reaction. — 
The conditions which cause variation in the knee-jerk we will 
now briefly enumerate. Absence of knee-jerk. — If after careful 
and repeated testing the knee-jerk cannot be obtained, disease 
is probably indicated. In most instances the disease is in the 
reflex arc itself. The constituent parts of this arc we have 
given above.* We will now mention some diseases which, 
by falling upon the various parts of this arc, may abolish the 
knee-jerk. The whole of the lumbar enlargement may be 
attacked by myelitis (AE) ; f the lumbar motor cells by 

* Vide p. 21. The spinal centre (which must be intact to allow of the 
presence of the knee-jerk) is in the upper lumbar region (2d to 4th seg- 
ment : Gowers). 

I In this enumeration (A) denotes that the disease attacks the afferent 
part of the arc, (E) the efferent, (AE) both parts. Disease of the efferent 
part is usually accompanied by muscular weakness or wasting, or electrical 
abnormalities. Disease of the efferent part may or may not be accompanied 
by sensory disturbances. In peripheral neuritis the nerve-endings to the skin 
may escape while those in the tendons are involved ; and again in intra- 
spinal disease the afferent fibres to the brain may escape while those to the 
reflex spinal centre are diseased. In such cases the tendon-reflex may dis- 
appear, without any loss of cutaneous sensibility. 



METHODS OF INVESTIGATION. 1 1 I 

anterior cornual myelitis (E), as in infantile spinal paral- 
ysis ; the intra-spinal afferent nerve-fibres by posterior scle- 
rosis, as in tabes dorsalis (A) ; the extra-spinal nerve-roots by 
meningitis (A or E or AE) ; the nerve-trunks by neuritis 
(AE) ; the nerve-endings by peripheral neuritis (A or E or 
AE) ; the muscles by primary myopathy (E). 

On the other hand, the knee-jerk may be present but may 
be feeble or exaggerated; but as it varies much in different 
persons, even in health, experience alone, aided by a careful 
consideration of the other factors of the case, must determine 
whether the feebleness or exaggeration is morbid. Mere 
feebleness (unless it be unilateral, or unless the feebleness has 
developed under observation) is not as a rule of much diag- 
nostic importance. 

Exaggeration of the knee-jerk implies, at least, that there 
is no destructive lesion of the reflex arc, and probably also 
that the reflex centre is over-active. The precise cause for 
such over-activity is doubtful. The conditions under which 
it is found are the following: either (i) without concomitant 
organic disease, as in hysteria, in certain stages of epileptic 
fits, in early hemiplegia, or in strychnia-poisoning (Charcot) ; 
or (2) with organic disease, commonly in the form of sclerosis 
of the pyramidal tract (lateral sclerosis). Such sclerosis may 
be bilateral, either secondary to a transverse lesion of the 
cord higher up, or (possibly) idiopathic and primary in both 
lateral columns. The tendon-reflexes are then exaggerated 
on both sides. Or the sclerosis may be unilateral, secondary 
to a lesion in the opposite cerebral hemisphere ; the tendon- 
reflexes are then exaggerated on one side only.* With such 
lateral sclerosis three main symptoms are usually associated : 

(1) paralysis or paresis from interruption of the motor tract; 

(2) exaggeration of the tendon-reflexes, and (3) when the 
sclerosis is well-developed, rigidity of the paralyzed limbs. 

*In yet another form of sclerosis — namely, disseminated sclerosis — the 
tendon-reflexes are usually exaggerated. 



I 12 NERVOUS DISEASES. 

Rigidity or Contracture of Muscles. — Rigidity is a 
striking symptom and must be further considered. It is 
closely associated with exaggeration of tendon-reflex, which 
latter symptom not only accompanies, but often is the pre- 
cursor of rigidity. Rigidity, like exaggerated tendon-reflex, 
may appear independently of anatomical lesion in the cord, 
or else may be the index of lateral sclerosis. Both varieties 
may sometimes be seen in a case of cerebral hemorrhage. In 
the early stage of this disease, before the cord has become 
sclerosed, there may be rigidity which will probably pass off. 
This is presumably due to cerebral irritation, and is called 
' ' early rigidity. " " Late rigidity " is a subsequent and more 
permanent phenomenon, and comes on when secondary lat- 
eral sclerosis of the cord has followed upon the original cere- 
bral lesion. This rigidity depends on continuous muscular 
contraction, which exists to a certain extent in all the para- 
lyzed muscles, but predominates in some groups. Thus, in 
the leg the usual effect is to produce extension of the leg 
and thigh with some adduction and internal rotation of the 
thigh ; in the upper limb, semiflexion with semipronation of 
the forearm, adduction of the upper arm, with flexion of the 
fingers into the palm. Thus rigidly extended lower limbs 
with the knees pressed together are suggestive of bilateral 
spinal sclerosis ; stiffness of one leg, with the attitude just 
described of the corresponding upper limb, is characteristic 
of old hemiplegia. 

Abnormalities of Tendon-Reaction apart from Dis- 
ease of the Reflex Arc. — In considering the association 
of lateral sclerosis with the knee-jerk, we have already passed 
beyond the consideration of the reflex arc itself. There is, 
indeed, little doubt that the tendon phenomena can be pro- 
foundly influenced by the higher (intra-cranial) centres. 
Experimental physiology would lead us to think that such 
influence is inhibitory — i.e., that those higher centres hold 
the spinal reflex centres in check, and that the removal of 



METHODS OF INVESTIGATION. I I 3 

their influence allows the reflex-action to become excessive. 
In man this may be also true : for, as we have seen, the knee- 
jerk is excessive in lateral sclerosis, and one effect of such 
sclerosis is to obstruct the downward path from the brain. 
But other facts indicate that the cerebral influence is neces- 
sary, not merely for control, but also for production of ten- 
don-reflexes. Thus, after an epileptic seizure there is a stage 
when the tendon-reflexes are absent, which precedes the stage 
of exaggeration. Again, absence of tendon-reflexes may be 
sometimes seen in cerebral tumor, and still more commonly 
in cerebellar tumor. Lastly, Bastian, Bowlby, and Thorburn 
have shown that if the spinal cord be completely divided by 
disease or injury, the lower limbs are flaccid and the tendon- 
reflexes absent, and this, though the lumbar centres be intact, 
and even though there be descending lateral sclerosis. 

Ankle-clonus. — Tendon reactions, like skin reflexes, may 
be elicited in very various parts of the body. In the lower 
limb, next to the knee-jerk in importance comes the phenom- 
enon of "ankle-clonus."* This, when present, is elicited 
as follows : let the patient's knee be slightly flexed, and 
support it, if necessary, with one hand in that position. 
Then with the other hand press the toes rather suddenly 
upward so as to cause dorsiflexion of the foot and toes, and 
maintain a certain pressure on them. The calf muscles will 
contract in response to the pull on their tendon, and will 
point the foot down again. They then relax; but the con- 
tinued upward pressure of the hand causes them to contract 
again. Thus a rhythmical oscillation of the foot is kept up,- 
which is called "ankle-clonus" or "foot-clonus." Some- 
times the mere pressure of the toes on the ground may start 
such a clonus ; and it may continue till the calf-muscles are 
permanently relaxed by forcibly pointing the foot downward. 

* Centre at junction of lumbar and sacral regions. 



I 14 NERVOUS DISEASES. 

Unlike the knee-jerk, ankle-clonus is not present in health ; 
it is to be regarded as an exaggerated tendon phenomenon. 

The "front-tap" contraction, also an exaggerated tendon 
reaction, is produced by percussing midway between the 
tibia and fibula about two-thirds down the front of the leg ; 
the response is a contraction of the calf-muscles, and conse- 
quent downward pointing of the foot. 

In the upper limb there are certain tendon phenomena 
often to be seen in health, and marked in cases of disease. 
The triceps cubiti may be made to contract as follows : 
support the upper arm so that it makes an angle with the 
trunk, and so that the olecranon is directed outward, letting 
the forearm hang vertically; then percuss the triceps tendon. 
Or a jerk may be obtained at the wrist, thus : support the 
forearm in a position of slight flexion, and tap the lower end 
of the radius, the biceps cubiti and supinator longus will 
contract and jerk the forearm and hand slightly upward. 

In cases of exaggerated tendon reaction, a contraction has 
been elicited in the temporal and masseter muscles, by depres- 
sing the lower jaw with a smart tap. This has received the 
euphonious name of "jaw-jerk." 

Inco-ordination or Ataxy of Movement.— Move- 
ments, even of a simple kind, are rarely executed by the 
contraction of one muscle, but by the combined contraction 
of several. Unless these various contractions be properly 
adjusted to each other in time and in force, the movement 
becomes awkward, irregular, or even impossible. Such a 
want of adjustment is called " inco-ordination," or sometimes 
"ataxy." It may be manifest not only in movement (motor 
ataxy), but in the combination of muscular contractions 
necessary to retain a fixed position, say that of standing 
upright; and it may then be called " static ataxy." Both 
kinds of defect may be shown in walking (locomotor ataxy), 
because for walking the balance of the trunk must be kept, 



METHODS OF INVESTIGATION. I 1 5 

and the legs moved harmoniously at the same time. Inco- 
ordination of movement may be caused by defects of various 
kinds. In the case of such movements as are primarily vol- 
untary and subsequently reflex, it is seen at the stage when 
the reflex centres are imperfectly educated. Thus an infant's 
walk is ataxic. But after the movement has been perfectly 
acquired (that is, become reflex), the balance of muscular 
action may be disturbed (1) by defect on the motor side, in 
consequence of which the call made by the centre on the 
muscles is unequally responded to ; (2) by defect in the 
afferent apparatus, in consequence of which the centre is 
misinformed of the position of parts, and therefore directs 
wrongly. In this latter case the muscular sense, whereby we 
know the position of our limbs, is usually at fault, and the 
patient will try to correct this by the aid of sight ; but if he 
be made to shut his eyes, his ataxia becomes evident. If, 
as frequently happens, the sense of touch is at fault also, the 
ataxia will be still further aggravated. Inco-ordination may 
be also seen in movements which we should at first call purely 
voluntary. There may be two reasons for this. First, 
because the defect may be, as just said, motor, and therefore 
interfering with calls from higher and lower centres alike ; or 
secondly, because in almost every action the muscular adjust- 
ment is a reflex matter, though the stimulus to action may be 
a matter of volition. 

Vertigo is the feeling we experience when our perceptions 
of our relations in space to surrounding objects are discordant 
or confused. In this general sense it probably corresponds to 
the popular term "giddiness;" but in a more definite sense 
vertigo is said to mean the sensation that we ourselves are 
moving, or objects around us moving, when no such motion 
exists. When vertigo is severe, the abnormal sensation is 
followed by actual movement, and the patient who felt himself 
turning actually does rotate, or he who feels giddy actually 
falls to the ground. In inquiring after vertigo we should 



Il6 NERVOUS DISEASES. 

endeavor to make the patient distinguish giddiness from a 
mere sense of faintness; and if he actually experiences a 
sense of movement, we should inquire in what direction this 
movement seems to be. 

There are varieties of vertigo which depend on different 
causes. Ocular vertigo results from partial paralysis of an 
ocular muscle. Our judgment of the direction of an object 
largely depends on the effort made in the ocular movement 
for fixing it. In partial paralysis of an ocular muscle, the 
patient makes an extra effort to fix an object and hence judges 
wrongly of its position ; if he tries to touch it quickly, he 
misses it. If he walks, the misjudging of his surroundings 
makes his gait unsteady, and (subjectively) causes him vertigo. 
These symptoms disappear when the paralyzed eye is closed. 
Aural vertigo is very common ; it is a purely sensory defect. 
One division of the labyrinth — viz., the semicircular canals, is 
appropriated to the perception not of sounds, but of the 
varying positions of the head according as we lie down, stand 
upright, or incline the head in any direction. The varying 
pressure of the endolymph in the ampullae is thought to fur- 
nish the stimulus, and the impressions are probably conveyed 
by a definite part of the auditory nerve. The constant and 
correct reception of such impressions is obviously most 
important for the maintenance of equilibrium. Disease of 
the middle ear which affects the labyrinth secondarily, disease 
of the labyrinth itself, of the auditory nerve, or of its central 
connections, may therefore produce vertigo. This may either 
take the form of a chronic giddiness and unsteadiness, usually 
with exacerbations, or there may be paroxysmal attacks, 
sometimes of great severity, in which the room or the bed, or 
the patient himself, seems to him to be turning round, tossing 
up and down, or rushing through space. There are additional 
symptoms: (i) vomiting and collapse, perhaps due to exten- 
sion of the irritation to the nuclei of the vagus ; (2) tinnitus 
and deafness, which indicate the aural origin of the affection. 



METHODS OF INVESTIGATION. WJ 

Such paroxysmal attacks of vertigo with tinnitus, vomiting, 
and collapse, associated with a progressive deafness for which 
no cause can be found in the middle ear, constitute the train 
of symptoms known as Meniere's disease. Aural vertigo 
is not remedied by closing the eyes ; it may occur even while 
the patient is in bed. Movements of the head (<?. g., turning 
over in bed) may bring on the attacks. Except in the mild 
cases where it is diluted down to a mere giddiness, the sense 
of movement is well marked and definite in direction. Where 
there is a sense of rotation, this is usually toward the side of 
the diseased ear. 

Gastric vertigo (vertigo a stomacho laeso) is said to arise 
from digestive disturbance, but its existence is denied by some 
eminent authorities. ' 

Epileptic vertigo occurs either as the prelude to a fit, or 
as the substitute for a severe fit (petit mal). It has these 
resemblances to aural vertigo, that it is paroxysmal and often 
definite as regards the direction of the apparent motion. 
When associated with definite epileptic fits the diagnosis is 
easy ; but this may be difficult where there is petit mal only. 
The purely epileptic vertigo will probably be of shorter dura- 
tion than the aural ; there will be no other aural symptoms, 
but there may be pallor, slight loss of consciousness, and 
perhaps some spasm even in mild attacks, whereas it is only 
in severe aural cases that symptoms of this kind occur. But 
we must not forget that the two causes, epilepsy and ear dis- 
ease, may both co-operate. The actual rotation of head, 
eyes, or body, that follows an attack of epileptic vertigo, is 
usually toward the side to which the patient fancied himself or 
his surroundings to be turning. The pupil of this side may 
be a little larger than the other. 

These are the most definite forms of vertigo, but the symp- 
tom may occur in a variety of nervous diseases. It is evident 
that the function of equilibration depends on a large number 



I I 8 NERVOUS DISEASES. 

of peripheral organs, and must therefore be represented in a 
large area of the central nervous system. 

Speech Defects. — Defects of speech make an important 
contribution to the symptomatology of nervous diseases. We 
will, first of all, distinguish three classes of such defects. 

(i) Articulatory. — The first class embraces speech affec- 
tions which depend solely on difficulty of articulation. The 
examples are somewhat various ; the nasal indistinct speech 
(especially indistinct for labials) of bulbar paralysis ; the 
drawling inarticulate speech which often accompanies hemi- 
plegia; the hesitating confluent speech of general paralysis; 
and the peculiar "scanning" or " syllabic" speech of dis- 
seminated sclerosis, in which words and syllables are brought 
out slowly and with separation. To these articulatory defects 
the name "aphemia" has been given. (2) In the second 
class of speech defects the patient's articulation (for such words 
as he may still possess) is not at fault ; but he has lost the 
power of expressing his thoughts by language. Thus he is 
unable, in extreme cases, to say any words, or his speech is 
limited to some routine words or phrase, or he misuses words. 
But he still has a correct mental vocabulary, for he under- 
stands what is said to him, knows when he himself has spoken 
wrongly, and his reasoning powers are unimpaired. Only he 
cannot use his words for purposes of speech; the "way out 
for words " (as it has been said) is blocked. This defect is 
called "aphasia" (in the limited sense of that term), or 
sometimes " motor aphasia; " or " Broca's aphasia," because 
the anatomical lesion corresponding to it — viz., in the pos- 
terior part of the third frontal convolution of the left cerebral 
hemisphere — was first localized by Broca. (3) The third 
class of defects is called " amnesia " (more fully, amnesia 
verborum), because the patient has lost the memory of spoken 
words. Words addressed to him are no longer symbols, call- 
ing up appropriate groups of ideas ; nor can he group his own 



METHODS OF INVESTIGATION. II9 

ideas under their appropriate symbols in speech. Therefore, 
though he hears what is said to him he does not understand it ; 
though his power of utterance is not lost, like the aphasic, his 
utterances may be confused and unintelligible both to others 
and himself; and his reason is impaired through failure of the 
mental imagery of words. This condition has also been 
called "word-deafness," or " sensory aphasia." The position 
of the lesion is less certain than in aphasia proper ; probably 
it lies somewhere near the auditory centre in the neighborhood 
of the posterior end of the fissure of Sylvius, on the left side 
of the brain. 

Thus, with respect to spoken language, we may reasonably 
recognize two cortical areas or "centres," the one devoted 
to the reproduction of words in speech, and therefore pre- 
siding over the (lower) articulatory centres; the second de- 
voted to the reception and storage of spoken words, being 
fed, so to speak, from the organ of hearing. For written 
language we are tempted to assume a similar pair of centres, 
the one for the expression of thought in writing, the second 
for the storage of visual memories of written (or printed) 
words ; seeing that similar defects have been described on the 
visual side — viz., an inability to communicate ideas by writ- 
ing, or " agraphia," corresponding to aphasia; and an in- 
ability to comprehend written or printed matter, due to loss 
of the visual memories of words, or word-blindness. 

It remains to be added that for perfect speech not only is 
the action of some such centres required, but their combined 
actions. Hence there may be (4) varieties of speech-defects 
due to lesions, not in the cortical centres themselves, but in 
the fibres connecting them (" commissural aphasia"). 

Coma. — A patient who appears to have lost consciousness, 
and to be able neither to feel, nor speak, nor move voluntarily, 
and who on recovery has no memory of his past condition, is 
said to be in a state of coma. There are various degrees of 
such a state. In the minor forms, called hebetude or stupor, 



120 NERVOUS DISEASES. 

there is little more than dulling of the mental faculties ; the 
patient may tell his name when asked, may put out his tongue 
when told, etc., but he volunteers nothing, cannot give long 
answers, and tends to lapse into a somnolent condition. In a 
state of deeper unconsciousness he neither answers nor ap- 
pears to hear, his eyes wander aimlessly when opened, but he 
still may stir when touched, or even perform quasi-voluntary 
actions, and the reflex actions still go on. In still deeper 
coma the breathing becomes stertorous from paralysis of the 
palate, the optic axes may diverge, and reflex actions begin 
to fail, so that he cannot swallow, and has no longer control 
over the sphincters. This stage is usually the prelude to cessa- 
tion of the respiratory and cardiac movements — i.e., to death. 
Congestion of the lungs, accompanied by a continuous and 
considerable rise of temperature, is often the immediate cause 
of death. 

The causes of coma may be very various, and the prognosis of 
a case varies much, according to the cause at work. But from 
the physical state of the patient, without an accurate history 
of the conditions which led up to the attack, it may be dif- 
ficult or impossible to diagnose the cause. The only safe rule 
in such a case is to wait and watch, taking such measures to 
empty the stomach and intestines as will not, by too violent 
action, aggravate possible cerebral disease. The causes of 
coma may be roughly "classed as functional, toxic, and or- 
ganic. Under the head of functional coma come cases due to 
hysteria, epilepsy, insolation, and to diseases such as dissem- 
inated sclerosis, general paralysis, and the like, which indeed 
present organic lesions, but none sufficient to account for the 
coma at that particular time. The prognosis in most func- 
tional cases is favorable. Toxic coma forms a common class 
of cases, all the more important because prompt remedies, 
such as emptying the stomach or bowels, or the administration 
of antidotes, may be needed. Acute alcoholism is perhaps the 
commonest ; next, poisoning by opium and other narcotic 



METHODS OF INVESTIGATION. 121 

drugs. Under this head also may be ranked ursemic and 
diabetic coma. Lastly, coma may be caused by almost any 
organic disease of the brain ; and it is the more likely to 
follow in proportion as the cerebral disease is (i) sudden in 
onset, (2) extensive. Cerebral hemorrhage is a very common 
cause ; cerebral embolism or thrombosis a less frequent cause ; 
meningitis, tumor, abscess, produce coma chiefly in their 
later stages. Into the differential diagnosis of the various 
conditions which we have enumerated we cannot now enter. 

There are other general symptoms due to morbid states of 
the nervous centres to which we need only make allusion, 
such as delirium, a symptom fully treated of in books on 
general medicine ; and insanity, which forms the subject of 
special treatises. 



CHAPTER IV. 

SYMPTOMS REFERABLE TO THE ORGANS 
OF SPECIAL SENSE. 

THE EYE. 
Ocular Paralysis. — It is obvious that to understand 
paralyses of the ocular movements we must have some 
knowledge of the action of the ocular muscles. The following 
account of their action is taken chiefly from Dr. Bristowe's 
excellent text-book of medicine. To each eyeball six muscles 
are attached — viz., external and internal rectus, superior and 
inferior rectus, inferior and superior oblique. Let us now 
take three axes drawn each through the centre of the eyeball, 
when the eye is at rest and looking straight forward horizon- 
tally (Fig. 35)— 

Viz., A A, a vertical axis; 

00, a horizontal axis, drawn outward and forward 
from the inner side of the optic disc to the outer 
margin of the cornea ; 
RR, another horizontal axis, nearly at right angles to 
00, coming out in front near the inner can thus. 
Then the action of the external and internal recti is to 
rotate the eyeball round the vertical axis AA, the external 
rectus in the outward direction, the internal in the inward. 
The oblique muscles rotate it round the axis 00, the inferior 
giving it an upward movement, the superior a downward. 
The superior and inferior recti rotate it round the axis RR, the 
superior giving it an upward, the inferior a downward move- 
ment. The movements imparted to the cornea by these 
various muscles are as follows : by the external and internal 

122 



THE EYE. 123 

recti, simple outward or inward movement respectively; by 
the obliqui, movements differing according to the position 
from which the cornea starts, but always along the concentric 
circles, in Fig. 36, of which O is the centre; by the superior 

Fig. 35. 
A 



FL 

A 

Diagram to Show Axes op Rotation Produced by the Ocular Muscles (Left 
Eye). {Modified from Bristowe.) 



and inferior recti movements which vary in the same manner, 
but always along the concentric circles, of which J? is the 
centre. Thus, supposing the eye to be looking along the axis 
00, the obliqui will give no movement to the cornea save 




Diagram to Show the Lines of Movement Produced by the Recti Muscles 
(Superior and Inferior), and by the Obliqui (Superior and Inferior Re- 
spectively). Left Eye. (After Bristowe) 



that of rotation, but the superior and inferior recti will give 
an up and down movement respectively. Suppose it to be 
looking along the z.y\%RR, then the superior and inferior recti 
will only give a rotatory movement, but the oblique will give an 



124 NERVOUS DISEASES. 

up and down movement. Suppose, again, the eye is looking 
straight forward, then acting singly, 

The inferior oblique will move the cornea upward and outward, in the 

direction of the upward 
single arrow. 

The superior oblique " " " downward and outward in the 

direction of the downward 
single arrow. 

The superior rectus " " " upward and inward in the 

direction of the upward 
double arrow. 

The inferior rectus " " " downward and inward in the 

direction of the downward 
double arrow. 

There will be in each case a tilting of the vertical meridian 
of the cornea ; for this meridian preserves the direction of the 
concentric circle along which the cornea moves. 

But to carry the cornea directly upward from the original 
central position, a combined action is necessary on the part 
of the superior rectus and inferior oblique ; and to carry it 
directly downward, a similar combination between the inferior 
rectus and superior oblique ; the motion being in each case 
the resultant of the action of the two muscles. 
. Ocular paralysis is chiefly recognized by the following 
symptoms: defective ocular movement ; squint or want of 
correspondence between the optic axes ; diplopia or double 
vision. 

Defective movement is recognized by making the patient 
follow with his eyes an object moved in various directions ; 
the affected eye lags behind the other when the movement to 
be elicited requires the action of the paralyzed muscle. Thus, 
when the object is moved in the direction of the muscle's 
action, it may be easy, in simple and well-marked cases, to 
recognize the nature of the paralysis. 

The squint, which is simply the result of the defect of 
movement, is recognized by the same means. Squint may 
exist, however, even when the eyes are at rest, owing to the 
unbalanced action of the muscles which antagonize those that 
are paralyzed. The eye squints in a direction opposite to the 
line of action of the paralyzed muscle. 



THE EYE. 125 

The diplopia is caused by the non-correspondence of the 
optic axes. Owing to this the images from the object fixed 
do not fall on corresponding points in the two retinae ; and 
are therefore referred to different directions in space. In 
Fig. 37 the left eye is squinting inward, and therefore rays 
from a distant object which in the right eye fall on the macula 
lutea, fall in the left upon a point internal to this. But since 
the internal half of the retina would receive under normal 
conditions rays from objects in the outer half of the field of 

Fig. 37. 





Diagram to Illustrate Squint prom Paralysis of Left External Rectus. 

The object fixed is supposed to be in the distance, and the rays from it are parallel. 
These coincide with the principal axis, PM, of the right eye, but not with that of the 
left. M, macula lutea. i i, internal half of each retina corresponding to external 
half of its visual field, e e, external half of each retina corresponding to internal 
half of its visual field. The arrow shows the direction in which the false image is 
displaced. 

vision, the image formed in the squinting eye is referred to a 
place external to (i.e., to left of) its real position. This is 
called the false image; it is generally fainter than the other 
one because it is formed further from the macula lutea.* The 
displacement of the false image is in the opposite direction to 



*If there is any doubt as to which image belongs to which eye.it may 
be settled by using a candle-flame for object and making the patient hold a 
colored glass in front of one eye. 
1 1 



126 NERVOUS DISEASES. 

the squint, and, therefore, in the direction of the line of 
action of the paralyzed muscle. Diplopia is said to be crossed 
when the false image is diplaced toward the side of the non- 
paralyzed eye ; homonymous when it is displaced toward the 
side of the paralyzed eye. Just as the amount of squint 
increases as the patient attempts to utilize the paralyzed 
muscle, so does the divergence of the images ; but since the 
false image is brighter the nearer it is formed to the macula 
lutea, it may happen that the diplopia is then most troublesome, 
when the squint is barely perceptible. 

We may add this, that the patient often attempts to correct 
the squint by turning his head in the direction in which the 
paralyzed muscle ought to carry the eye, so that sometimes the 
nature of his complaint can be guessed at once. Of vertigo 
from ocular paralysis we have already spoken. 

Two examples may be given of paralysis of an individual 
ocular muscle. 

Left External Rectus. — Innervation from sixth nerve: 
action, turns eye horizontally outward (to left). 

Symptoms of paralysis; left eye lags or is immobile when 
patient looks to left ; left eye squints inward ; false image is 
placed to left of true image (homonymous diplopia), and is 
on the same plane with it, and is not tilted. 

Left Superior Oblique. — Innervation from fourth nerve ; 
action (supposing the eye to start from a position of rest) 
carries the cornea downward and to left, at the same time 
tilting the upper end of its vertical meridian inward (to 
right). 

Symptoms of paralysis; squint little or none as the eye 
looks straight forward, but if the patient attempts to look 
downward (or, still more, if downward and to left), the left 
cornea remains rather above and to right of the position it 
should take up, and also appears to screw round slightly in 
the direction of the hands of a watch ; homonymous diplo- 
pia (on looking downward and to left), the false image being 



THE EYE. 



127 



placed below and to left of the true, and its upper end tilted 
to right. 

All the remaining muscles of the eyeball, and also the elevator 
of the upper lid, are supplied by the third nerve. Complete 
paralysis of the third nerve-trunk causes the following symp- 
toms : ptosis — i. e., closure of the eye from inability to raise 
the upper lid ; loss of movement of the eyeball, except the 
outward movement (supplied by the external rectus and sixth 
nerve), and the downward and outward movement (supplied 
by the superior oblique and fourth nerve) ; external squint 
with crossed diplopia. Further, the pupil is somewhat larger 
than that of the sound eye, and does not contract under the 
stimulus of light or of accommodation effort, because the 
third nerve supplies the sphincter pupillse ; and the power of 
accommodation is also lost, because the third nerve supplies 
the ciliary muscle. Syphilis is a frequent cause of paralysis 
of the third nerve. This, or indeed any form of ocular par- 
alysis, may occur in the early stages of tabes dorsalis, or less 
frequently of disseminated sclerosis ; in these cases the par- 
alysis is generally transient. Recurrent ocular paralysis may 
occur in connection with migraine. 

Complex Ocular Paralysis.— But ocular paralysis is by 
no means always limited to one muscle, or the muscles supplied 
by one nerve-trunk. It may affect simultaneously several 
independent muscles, or muscles of the two eyes, or there 
may be loss of particular movements rather than paralysis of 
any particular muscles. Such complicated ocular paralysis 
may be produced in various ways : (1) By peripheral neuritis 
in the district of the oculo-motor nerves, an example of 
which is to be found in the ocular palsy which occasionally 
accompanies the limb paralysis of alcoholic neuritis. (2) 
By central disease affecting either the ocular nerve nuclei, or 
the root-fibres as they run from the nuclei toward their super- 
ficial origin. If such disease be a coarse lesion, such as a tumor, 
hemorrhage, etc., it will probably produce other symptoms 



128 NERVOUS DISEASES. 

besides ocular palsy, most likely cross paralysis {vide p. 95), 
and the ocular paralysis will often be bilateral, seeing that the 
nerve nuclei and root-fibres, at any rate those of the two 
third nerves, lie near together. If the disease be microsco- 
pic — viz., a chronic degeneration of the oculo-motor nuclei, 
the symptoms are still more likely to be bilateral. Such 
nuclear disease is usually chronic and progressive, and it gives 
rise to the set of symptoms known as progressive ophthalmo- 
plegia — ophthalmoplegia externa when the movements of the 
eyeballs gradually fail ; ophthalmoplegia interna when the 
movement of the pupil and the power of accommodation 
are affected. Such ophthalmoplegia is analogous to the pro- 
gressive muscular atrophy which depends on degeneration of 
the anterior cornual cells of the spinal cord, and indeed it 
may actually be accompanied by muscular atrophy, or may 
form a part of some other spinal degeneration, such as tabes. 
An acute affection of the region of the third nucleus has also 
been described, of rare occurrence, probably inflammatory in 
nature, occurring generally in drinkers, associated with symp- 
toms of delirium tremens, and ending fatally. 

There may be loss of a combined movement of the two 
eyes, the muscles engaged being paralyzed for that movement 
only, and not for other movements. Take, for example, the 
movement of directing the two eyes laterally to the left. 
This requires a combined action on the part of the left 
external rectus and the right internal rectus ; and it may be 
that the two muscles are powerless for this purpose, though at 
the same time the internal rectus retains its power for other 
movements, such as that of convergence. For the lateral 
movement just described the two muscles are said to be 
"yoked" or "conjugate," and the movement is called a 
conjugate movement, or, more generally, an associated move- 
ment. It is believed that the sixth nucleus has such connec- 
tions with the external rectus of the same side {via the sixth 
nerve-trunk), and with the internal rectus of the other side {via 



THE EYE. 129 

the third nucleus and nerve-trunk) as enables it to produce 
the aforesaid conjugate movement of the eyes to the same 
side. Destruction of one sixth nucleus will consequently 
produce loss of conjugate movement of the eyeballs toward 
the side of the lesion. 

Such movements are dependent also upon higher centres in 
the cerebral hemisphere. Experiment shows that in the 
cortex of each cerebral hemisphere in the monkey there is a 
centre or centres, the action of which is to cause turning of 




Diagram to Illustrate the Mechanism of Conjugate Lateral Movements of 
the Eyes. 

C, Cortical centre, stimulation of which causes rotation of both eyes toward opposite 
side, and paralysis of which allows conjugate deviation to the same side. Nvj, 
Nucleus of 6th nerve, connected by the fibres of the 6th nerve (vj) with the 
external rectus (e) of the eye of the same side, and through the opposite 3d 
nucleus {Niij) and 3d nerve (iij) with the internal rectus (/) of the opposite side. 



the eyes and head to the opposite side. In hemiplegia from 
cerebral disease in man, there is often a turning (conjugate 
deviation) of the head and eyes. They turn usually away 
from the side of the hemiplegia, and therefore toward the 
side of the lesion. The explanation given is that the cortical 
centre upon the side of the lesion being destroyed, or cut off 
by lesion of its sub-cortical fibres from the parts below, the 
action of the opposite cortical centre is unbalanced, and there- 



I30 NERVOUS DISEASES. 

fore the head and eyes look toward the side of the lesion. 
Probably the fibres from each such cerebral centre descend, 
cross, and finally end in the opposite sixth nucleus.* Thus, 
a paralyzing disease in the right cerebral hemisphere would 
cause conjugate deviation toward the right, while in the right 
side of the pons it would cause conjugate deviation toward the 
left; but an irritative disease (i. e., such as caused undue 
stimulation) in either locality, would produce just the reverse 
effects. 

There are other associated movements of the eyes which 
may be lost in disease, such as the movement of convergence, 
and the movement of looking upward. 

Nystagmus. — Sometimes the eyes, instead of remaining 
steady when directed toward an object, or instead of following 
a moving object equably and steadily, exhibit continuous 
jerks or small oscillations. This condition is called nystagmus. 
It may arise (apart from actual nervous disease) from defects 
of vision either congenital or dating from early childhood or 
in connection with some continuous strain upon the ocular 
muscles, as in "miners' nystagmus." Nystagmus arising 
from nervous disease is said to manifest itself more when the 
eyes are used for fixing or following an object than when they 
are at rest. The minor degrees of it are certainly best demon- 
strated by making the patient fix an object far to one side of 
him, thereby putting some strain upon the muscles. These 
jerky movements are (usually) present in both eyes ; they may 
be horizontal in direction, vertical, rotatory, or quite irregular. 
The nervous diseases in which nystagmus occurs are : dis- 
seminated sclerosis (toward the diagnosis of which it may 
contribute in an important degree) ; the variety of locomotor 
ataxy known as hereditary ataxy or Friedreich's disease ; 

* That is, the fibres which regulate the movement of the eyes : those for 
the movement of the head would, of course, end in the nuclei which act 
on other muscles. 



incomplete paralysis of the ocular muscles, as in tumors of the 
pons, peripheral neuritis. In disseminated sclerosis a fair 
comparison may be made between this tremor of the eyes and 
the tremor of the limbs. 

Paralysis of Pupil and Ciliary Muscle. — Leaving the 
movements of the eyeball, we come to the internal muscles of 
the eye. These are, (i) the ciliary muscle, (2) the sphincter 
of the iris, (3) the dilator of the iris. The last-mentioned 
muscle is innervated from the sympathetic, the other two from 
the third nerve. Sometimes all these muscles are affected by 
a paralysis, progressive in character, and depending probably 
on degeneration of the nerve-nuclei in the pons. This is 
called ophthalmoplegia interna ; it is analogous to, and may 
be associated with, the ophthalmoplegia externa which we 
have mentioned. Paralysis of the ciliary muscle only, the 
symptom being loss of accommodation, is most commonly 
due to diphtheritic paralysis.* It occurs in conjunction with 
other symptoms in paralysis of the third nerve. As to the 
pupils, in the natural state their apertures are circular, and 
equal on the two sides; the pupil contracts when light is 
thrown on the corresponding retina (reflex action), or on the 
opposite retina (crossed or consensual reflex) ; it contracts, 
too, with the effort of convergence or accommodation in 
looking at a near object (associated action) ; it dilates when 
the eye is shaded ; and dilates when pain is inflicted, as by 
severely pinching, pricking, or faradizing the skin of the neck. 
The size of the pupils varies with many circumstances ; they 
are often small in elderly people, large in myopic patients, 
large in states of excitement, or after the occurrence of an 
epileptic fit. An undue contraction of the pupils is called 
" myosis," the reverse condition " mydriasis." An important 
and early symptom of tabes dorsalis is often furnished by the 
pupils. The reflex contraction to light is not to be obtained, 

* Omitting, of course, presbyopia and conditions purely ophthalmic. 



I32 NERVOUS DISEASES. 

though there is still a contraction when the patient accom- 
modates. This is called reflex iridoplegia, or sometimes the 
"Argyll-Robertson phenomenon." Care must be taken in 
examining for it that the patient looks steadily into the 
distance all the time, otherwise the accommodation is exerted, 
and the associated contraction of the pupil appears. In some 
cases, however, even this associated action of the pupil is 
abolished, so that it is completely immobile.* Usually, 
though not always, the pupils in tabes dorsalis are small ; 
"spinal myosis" this is called. The movement of dilatation 
upon the application of painful stimuli is said to be abolished 
also, but this may be difficult to test. Tabes dorsalis is by far 
the most frequent cause of reflex iridoplegia, but it occurs 
sometimes in general paralysis of the insane, and occasionally 
in old syphilitic cases. 

In paralysis of the cervical sympathetic, the pupil of the 
affected side is a little smaller than the other one, since the 
sympathetic supplies the dilator fibres. Other symptoms of 
paralysis of the sympathetic are as follows : the eyelids droop 
somewhat, the eyeball appears retracted, so that the palpebral 
opening looks smaller than on the other side. Flushing and 
heat of the face upon the side of the paralysis may occur. 
Aneurisms, enlarged glands, tumors at the root of the neck 
or at the apex of the lung, may cause such paralysis of the 
sympathetic. The peculiarities of pupil may be seen in disease 
of the cervical or upper dorsal cord, or of the uppermost 
dorsal nerve-roots where the cilio-spinal fibres of the sym- 
pathetic leave the cord. 

Affections of Fundus Oculi.— It is hardly necessary to 
insist upon the importance of examining the fundus oculi. 
It is here only that we can directly inspect a nerve and its 
terminal expansions. Moreover, the condition of the optic 

* It should be ascertained that such immobility is not due to adhesions 
from old iritis, etc. 



THE EYE. I33 

nerve has a more than local importance ; it may furnish the 
best indication of central nervous disease. Thirdly, in the 
fundus oculi, as in other parts of the body, may appear 
symptoms of constitutional states, which need not necessarily 
be nervous in origin, but which may have important bearings 
on nervous disease, such as syphilis, Bright's disease, etc. 

For a description of the methods of ophthalmoscopic 
examination, and of those conditions of the media which 
must be taken into consideration in such examination, we 
shall refer the reader to text-books on ophthalmology. The 




Healthy Optic Disc, Erect Image. (From Nettleshij>, after Jager.) 

" direct " method is the easiest and best for the determination 
of minute changes in the fundus. 

The chief morbid conditions of the optic disc or papilla 
are: (1) Optic neuritis, or papillitis; (2) optic atrophy. 

Optic Neuritis. — In the normal condition the optic disc 
is circular, of translucent pink hue, variable in different per- 
sons, but almost always paler than the surrounding fundus ; 
its edge is distinctly traceable, generally more sharply marked 
at the sides than above or below, and particularly on the 
nasal side; the edge may or may not be bordered with pig- 
ment ; its centre (the lamina cribrosa) may be slightly de- 
12 



134 NERVOUS DISEASES. 

pressed, gray, and punctate in appearance; from the centre 
issue the retinal vessels, which mainly pass upward and 
downward, and then branch over the fundus. The veins are 
larger and darker than the arteries, and the vessels show a 
light streak running along their axis with a colored streak on 
each side, this " double contour " being due to the refraction 
of the light from their rounded surface. The nasal half of 
the disc is often paler than the temporal. 




Severe Optic Neuritis or Papillitis. {From Nettleship, after 
Hughlings Jackson.) 

In optic neuritis the color of the disc becomes at first 
deeper, approaching that of the fundus (congested or hyper- 
semic disc), though upon this alone much stress cannot be 
laid ; next, the edge of the disc, as seen by the direct 
method, becomes indefinable and hazy ; the haze, increasing, 
begins to obscure the vessels here and there; then swelling 
of the disc sets in, its central pit becomes filled up, the disc 
as a whole becomes raised above the level of the fundus ; its 
edges look frayed out and spread over the adjacent parts of 



THE EYE. 135 

the fundus. The swelling of the disc is evidenced by the 
difference of focusing required for it and for the fundus; by 
the difference in the apparent movement of the vessels on the 
disc and of those on the fundus as the observer's eye is shifted, 
by the curve of the vessels and their loss of double contour 
as they pass off the disc. As the swelling goes on the veins 
enlarge and become tortuous, the arteries become smaller ; 
hemorrhages may appear both upon and around the disc ; 
the neighboring parts of the fundus become involved in the 
haziness and swelling. This extreme condition of optic 
neuritis was formerly called "choked disc." 




Simple Atrophy of Disc. Stippling ok Lamina Cribrosa Exposed. (Fr 
Nettleship, after IVecker.) 



Optic Atrophy. — In optic atrophy the disc is no longer 
translucent, but has a dead opaque color, either chalky white, 
or dull gray, or yellowish. The central pit may appear either 
filled up, or more hollow than usual. In primary atrophy 
the edges of the disc are sharply cut ; when the atrophy is 
secondary to neuritis Cpost-neuritic or post-papillitic atrophy), 
the edges may remain ill-defined, at any rate here and there, 
and the vessels may be smaller than normal ; but this is not 
necessarily the case, and there may be no means of distin- 
guishing the secondary from the primary atrophy. Atrophy 
may be partial, but it must be remembered that even in a 



136 



NERVOUS DISEASES. 



normal disc the nasal half is apt to be paler, and its nasal edge 
more denned than the rest. 

Optic atrophy may be also secondary to various forms of 
retinitis, to embolism of the retinal artery, and other purely 
ocular affections. 

Fig. 42. 




Atrophy of Disc from Spinal Disease. Lamina Cribrosa Concealed, Ves- 
sels Normal. (From Nettleship, after Wecker.) 

Indications Afforded by Optic Neuritis or Atro- 
phy. — These affections of the optic nerve have a twofold 
bearing. First, upon the patient's vision. This is a question 

Fig. 43. 




Atrophy of Disc after Papillitis. (Nettleship.) 



principally for ophthalmic surgeons, and we shall only remark 
here that optic atrophy is almost always accompanied by im- 
pairment of vision, and may destroy vision altogether; but 
optic neuritis does not in all cases cause impairment. There- 



THE EYE. 137 

fore, the eyes should be examined, even when there is no 
complaint of loss of sight. Secondly, upon the presence of 
nervous disease elsewhere. Optic neuritis, affecting both eyes 
(double optic neuritis), is generally indicative of coarse 
organic disease within the cranium. The other symptoms of 
intra-cranial disease — headache, vomiting, convulsions, and 
even in some cases paralysis — may be due to purely functional 
causes ; but when optic neuritis is superadded, we may as a 
rule look for structural lesions, hence its importance in diag- 
nosis. Of such lesions, tumor is the commonest, either new 
growth in the strict sense (glioma, sarcoma, carcinoma) ; in- 
flammatory new growths, such as gummata and tubercular 
masses; or the rarer parasitic growths, such as hydatids, 
actino-mycosis, etc. The character of the tumor makes no 
difference to the optic neuritis; and as to locality, neuritis 
may accompany a tumor in any position. How the tumor 
causes the optic neuritis we do not fully know. Optic neuritis 
need not be present in all cases of intra-cranial tumor ; but it 
will probably be found at some stage or other of most tumors, 
if the eyes be frequently examined. Other organic cerebral 
lesions, which may cause optic neuritis, are, meningitis, ab- 
scess, or, it may be, thrombosis of sinuses, or hydrocephalus. 
It is very rarely present in cases of simple cerebral softening 
or cerebral hemorrhage. One or two cases have been de- 
scribed of optic neuritis in nervous diseases which were not 
intra-cranial — myelitis, disseminated sclerosis, peripheral 
neuritis; but these are also rarities. But it may be produced 
by causes quite outside the nervous system, such as Bright's 
disease, or perhaps anaemia. Hypermetropia, again, may 
cause appearances exactly resembling optic neuritis. 

Optic atrophy, we have said, may be primary or secondary 
to pre-existing neuritis. If secondary, it points to some of 
the conditions which we have just enumerated as causes of the 
neuritis, as either existing or having at one time existed. If 
primary, optic atrophy is usually connected with degenerative 



I38 NERVOUS DISEASES. 

disease of the spinal cord ; most commonly with tabes dorsalis 
(of which it may constitute a very early symptom), sometimes 
with the allied disease, general paralysis of the insane (spinal 
form), and also with disseminated sclerosis. Such atrophy 
may begin in one eye, but both are affected in time. There 
is a rare form of optic atrophy which seems to run in families. 

Affections of the other parts of the eye, even of the cho- 
roid and retina, have not the same direct bearing upon central 
nervous disease as have optic neuritis and optic atrophy. 
Nevertheless, an inspection of these parts may throw great 
light upon the constitutional condition of the patient, and 
thereby upon his nervous symptoms. Tubercles in the choroid 
may indicate the nature of a doubtful meningitis ; syphilis 
may be revealed by choroidal changes; Bright's disease by 
its characteristic retinitis. 

Affections of Vision. — The function of vision may be 
considered under the heads of central vision, the field of 
vision, and color-vision (central or peripheral). 

Of Central Vision. — When the eye is directed to any 
small object, which maybe called the "fixing point," the 
rays from this object fall on the yellow spot, and since this is 
the most sensitive spot in the retina, the object is seen with 
the greatest attainable clearness. This is central vision. When 
"acuteness of vision " without qualification is spoken of, the 
acuteness of central vision is meant. It can be accurately 
measured (when sufficiently good) by test types.* When too 
bad to allow of any type being read, it is judged of by the 
distance at which the patient can count fingers, or, in the 
worst cases, by his power of distinguishing light from dark- 

* Snellen's test-types are so constructed that each type can be read, when 
vision is normal, at a distance corresponding to the number of the types. 
Thus (if constructed for metres) when No. 6 is read at 6 metres, vision = g, 
i. e., is normal; when No. 6 is read at 3 metres, vision = {j, or half the 
normal, and so on. Small types, to be held by the patient, may be used, 
if we are satisfied that his accommodation is sufficiently powerful. 



THE EYE. I39 

ness. But simple diminution of acuteness of vision is more 
often than not due to disease of the eye itself; and therefore, 
before we proceed to associate it with central nervous disease, 
we must satisfy ourselves that the media, and more particularly 
the refraction, are not at fault, and that the ophthalmoscopic 
appearances of the choroid, retina, and optic nerve are healthy. 
The following are some of the causes of defective vision without 
demonstrable disease of the eye, and with little or no changes 
in the disc : toxic agents, such as tobacco, carbon bisulphide, 




Field of Vision of Right Eye for White and Colors on a Dull Day. 

(From Ross, after Gouiers.) 

The asterisk indicates the fixing point, the black dot the blind spot. 

quinine, perhaps alcohol, producing probably some neuritis; 
retro-bulbar neuritis — i. e., neuritis too far back to be visible 
ophthalmoscopically : central causes — uraemia, hysteria, mi- 
graine, epilepsy (temporarily), reflex irritation. 

Of Visual Field.— But disease of parts behind the optic 
nerve usually causes symptoms which have special relations to 
the fields of vision. The field of vision (Fig. 44), is the area 
around the fixing point within which objects can be perceived 



I40 NERVOUS DISEASES. 

without moving the eye. Each retina has its own field of 
vision ; in the centre is the fixing point which corresponds to 
the yellow spot of the retina, while the remainder corresponds 
to the more peripheral parts of the retina. Since the rays 
from objects in the field cross between the cornea and the 
fundus, the left half of the field will correspond to the right 
half of the retina, and vice versa, the upper half of the field 
to the lower half of the retina, and vice versa* The fields of 
the two eyes are symmetrical, they do not coincide exactly, 
for it is evident from their shape that the right half of the right 
eye's field overlaps the right half of the left eye's (and re- 
versely for the left halves), but they coincide in this sense, 
that rays from the same object (the fixing point being the 
same for both eyes) fall on corresponding points of both 
retinae — i.e., on points symmetrically disposed with respect 
to the yellow spot, to right or left of it, above or below. 
Taking then the visual field of the two eyes thus combined, 
and supposing it divided into two lateral halves, the right half 
of it will be perceived by the left half of either retina (inner 
half of right retina, outer half of left), and the left half of it 
by the right half of each retina (outer half of right, inner half 

* Examination of Fields of Vision. — A rough examination of the field 
may be made thus : — The patient closes one eye, and with the other fixes 
the corresponding eye of the examiner (so that the latter can see that the 
patient does not move his eye, and can at the same time contrast the 
patient's field with his own). The fingers of the examiner are then brought 
gradually from various points of the periphery toward the fixing point, and 
the patient has to say when they come into sight. For more accurate 
examination and recording, a perimeter must be used. A movable arm is 
made in the shape of a quadrant of a circle, and divided into angles; the 
patient's eye is placed at the centre of the circle, and the fixing point is 
at one end of the quadrant ; the object, usually a small square of paper, is 
made to travel along the quadrant, and the angle at which it becomes visi- 
ble is noted, and marked off on a diagram ; the quadrant can be rotated 
around the fixing point, and the process of estimating and recording the 
angle is thus repeated for as many meridians as is thought to be necessary. 



THE EYE. 141 

of left). Now, the disposition of the fibres proceeding from 
the lateral halves of each retina is as follows (Fig. 45) : — 

Those from the outer half proceed along the optic nerve- 
trunk in company with those from the inner as far as the 
chiasma; but here they part company, the fibres from the 
outer half of the retina going to the optic tract of the same 
side, the fibres from the inner half of the retina crossing over 
to the optic tract of the opposite side. Thus the optic tract 



Visual field of left eye 



Left eye 



Left optic nerve 
Chiasma 




Left optic 



Fibres to left an- / / ' ^ 
gular gyrus, j—j 



Fibres to left occi 
pital lobe. 

Diagram to Illustrate the Distribution of Fibres from the Occipital 
Lobes to the Lateral Halves of the Retin>e. 



w ■.— Right optic tract. 

\\ 

J \ \ Fibres to right 

: Y~l angular gyrus. 

• — Fibres to right oc- 
cipital lobe. 



of the right side contains the fibres from the right lateral halves 
of both retinae, and the optic tract of the left side contains the 
fibres from the left halves of both retinas. This arrangement 
is continued upward through the optic radiations of Gratiolet 
into the occipital lobes. Consequently, a lesion of one oc- 
cipital lobe or of the optic tract of one side produces blind- 
ness of the same named halves of both retina:, and loss of the 
opposite half of the field of vision. This is called " lateral " 



142 NERVOUS DISEASES. 

or "homonymous" hemianopia. Disease of the chiasma 
itself will damage the decussating fibres, and since these come 
from the inner half of each retina, there will be loss of the 
outer or temporal half of the field of vision in each eye (not 
corresponding halves, as in the last case). This is called 
" temporal hemianopia." Progress of disease at the chiasma 
may cause total blindness of both eyes. 

So far as regards the occipital lobes and the optic tracts, 
the scheme just given is fairly satisfactory. But in lesions of 
the angular gyrus,* and still more frequently in cases of hys- 
terical hemianesthesia, a different state of things is observed. 
The central vision of the eye opposite the lesion, or on the 
side of the hemianaesthesia, is diminished in acuity, perhaps 
almost abolished, and the field of vision is concentrically 
narrowed, while a similar but much less marked affection 
may be discovered in the other side. It would seem that 
each angular gyrus stands in relation to the vision, and par- 
ticularly the central vision, of the opposite eye, and in a less 
degree to that of the eye of the same side. Apparently each 
such centre (in the lower animals, at any rate) can supplement 
the action of the corresponding centre on the other side. 

Besides hemianopic defects and concentric narrowing, the 
fields of vision may be affected in other ways. A blind 
patch may appear in the centre of the field (central scotoma), 
or sector-like pieces of the field may be blotted out. Atrophy 
of the optic nerve is usually the cause of such affection. 

Of Color-Vision. — Color-vision may be affected in con- 
nection with, or independently of, other defects of vision. 
Some people, whose sight is otherwise good, are unable from 
birth to perceive certain colors. This constitutes congenital 
color-blindness; it is a defect that occasionally runs in 
families. Such a condition may be acquired; it is then 

* It must be noted, however, that the whole question of the relation of 
the angular gyrus to vision is still unsettled. 



THE EAR. I43 

generally due to optic atrophy, but may be also caused by 
hysteria or some cerebral lesion. Color- vision may be tested 
with sets of colored wools which are supplied for the purpose. 
In acquired color-blindness it may be sufficient to ask the 
patient to name the colors shown to him. But it is better to 
make him sort them into colors which seem to him unlike and 
like, or to match different colors chosen for the purpose ; being 
unable to perceive some one fundamental color, he will class 
as like some wools which to a normal eye appear different. 

There are visual fields for colors, as for white light (vide 
Fig. 44). These are less extensive than the field for white. 
The fields for colors may be concentrically narrowed (just as 
the fields for white) ; in some rare cases there may be hemi- 
anopia for colors. 

THE SENSE OF HEARING. 

Probably affections of hearing have as close a bearing on 
nervous disease as those of vision. But the deeper parts of 
the ear are not, like those of the eye, open to direct inspec- 
tion ; hence the investigation of them is the less easy, and has 
been less fruitful of result. 

The auditory nerve and its expansion in the labyrinth 
is devoted to two different functions: (1) that of hearing 
(cochlea) ; (2) that of receiving impressions necessary for 
equilibration (semicircular canals). Of disturbances of this 
second function we have already spoken under the head of 
"aural vertigo" (p. 116). It should be as natural to examine 
the ear in a case of vertigo as it is in a case of deafness. 

A definite and general standard of hearing has not yet been 
framed. The hearing distance is usually estimated by a 
watch. If a given watch is audible by a normal ear, say at 
24 inches, and the patient can only hear it at three inches, 
then the hearing distance of his ear may be expressed as ^, 
and so on. Each ear must (it is needless to say) be tested 
separately, the watch must be held vertically, and in a straight 



144 NERVOUS DISEASES. 

line with the ear. The hearing power is said to vary not as 
the hearing distance, but as the square of the distance. The 
watch test is open to the objection that different kinds of 
sound maybe heard with different degrees of distinctness; 
a patient who can hear the watch may be deaf to conversa- 
tion, and so on. It is evident that in this method of examina- 
tion the sound is conveyed from the watch by the air through 
the meatus to the membrana tympani, and thence via the 
ossicles to the labyrinth. This is called "aerial conduction," 
or it maybe called " meatal hearing. " But if a sounding 
body, such as the watch or a tuning-fork, be placed on the 
bones of the head (the forehead, vertex, mastoid process, or 
teeth), it is still heard even though the meatus be closed. 
This is called " perosseous conduction or perosseous hearing." 
The distinction between meatal and perosseous hearing may 
be used as a means of localizing the defect which causes 
deafness in a given case. If the deafness is due to disease of 
the external meatus, or of the tympanum, the perosseous 
hearing is not diminished, it may be even increased. (This 
fact may easily be verified thus : stop one external meatus 
with a moderate degree of pressure, and place a vibrating 
tuning-fork on the middle line of the forehead or vertex, the 
sound will be heard best in the ear which is closed.) But if 
the disease be in the labyrinth, auditory nerve, or nervous 
centres, both meatal and perosseous hearing are diminished 
pari passu. So that the tuning-fork placed on the middle 
line of the skull should be best heard with the diseased ear 
when the disease is peripheral (i.e., in the external meatus or 
tympanum), best heard with the sound ear when the disease 
is central (in labyrinth or nervous apparatus). But this test 
is perhaps less valuable than it appears to be, because (i) the 
patient's answers may be misleading; (2) both ears may be 
diseased ; (3) the disease may be both central and peripheral. 
Another test which may be useful is the following — it depends 
on the fact that the meatal hearing is normally more acute 



THE EAR. 145 

than the perosseous : place the tuning-fork on the mastoid 
process and let the patient say the moment when the sound 
ceases, then transfer the fork immediately and hold it just 
opposite the meatus. If the middle ear is sound, it should 
still be heard for a short time ; but if it is not so heard, 
disease of the middle ear is indicated. But still the fact 
remains that it may be very difficult, even after careful inspec- 
tion and careful testing, to eliminate the possibility of middle- 
ear disease, or to say, in the presence of some middle-ear 
disease, how much of a given deafness is due to it, and how 
much to central causes. 

There is a natural limit of the hearing power for notes that 
are very high pitched or very low pitched. This varies in dif- 
ferent individuals, with age, and perhaps with disease. Some 
people cannot hear the squeak of a bat or the chirp of a 
cricket. The range for high notes may be tested with Gal- 
ton's whistle. The total range of hearing for different notes 
has been compared to the field of vision. Perhaps it might 
be more accurately compared with color-vision. Abnormal 
limitation of this range, or a condition (sometimes observed) 
in which the patient is deaf to some intermediary notes, is 
usually held to be indicative of disease of the cochlea. 

Defective hearing is not uncommon in tabes ; but this may 
be often due to chronic middle-ear disease. Deafness may re- 
sult from disease of the auditory nerve (it may be the seat of 
new growth, and atrophy of it has been observed in tabes), 
or from disease of the pons, or from cerebellar tumor which 
has spread to the fourth ventricle. In such instances there 
will probably be paralysis of other cranial nerve-trunks. Uni- 
lateral deafness occurs in hysterical hemiansesthesia, or in dis- 
ease of the posterior extremity of the internal capsule. Deaf- 
ness from disease of the cortical centres requires further 
clinical investigation ; some cases, however, have been re- 
corded. Deafness from nerve-disease affects, as we have said, 
the perosseous as well as the meatal hearing. 



I46 NERVOUS DISEASES. 

Tinnitus, or noises in the ear, is a symptom that may be 
purely nervous, or may arise from disease of the ear itself; 
this must be determined by the accompanying conditions. 

SMELL AND TASTE. 

We need say but little concerning the senses of smell and 
taste. In testing smell we must not use such a substance as 
ammonia, the presence of which may be recognized by its 
irritating effects, apart from any smell proper; but rather 
such substances as musk, asafoetida, etc. The olfactory nerve 
is anatomically connected with the centre for smell (in the 
anterior part of the temporo-sphenoidal lobe) of the same 
side, but certain facts indicate that it is also connected with the 
centre of the opposite side. Disease of the anterior part of 
the temporo-sphenoidal lobe has in some cases been ac- 
companied by fits, which began with the sensation of a smell 
(or taste). 

In testing taste we must limit ourselves to the simple tastes 
of sweet, bitter, sour, salt (sugar, quinine, acids, salt). 
Elaborate flavors and aromas which we are said to " taste " 
are really distinguished by the sense of smell. Taste may 
be examined electrically, the nerve-ends being readily excited 
by a mild constant current applied by bared wires to the 
moist tongue. The nerves of taste are distributed to the 
tongue, palate, and fauces, in two areas: (1) the sides and 
tip of the tongue are supplied from the lingual branch of the 
fifth; (2) the back of the tongue, palate, and fauces are 
supplied from the glosso-pharyngeal. But the course of 
these fibres as they run toward the medulla is complicated. 
For (1) the lingual fibres pass up along the chorda tympani 
to the facial nerve, and run in it to the geniculate ganglion ; 
thence along the Vidian nerve (large superficial petrosal) to 
the spheno-palatine ganglion, and so along the second division 
of the fifth to its root. Thus disease of the lingual nerve 
near its termination, of the chorda, or of the facial between 



SMELL AND TASTE. 1 47 

the origin of the chorda and the geniculate ganglion, may 
cause loss of taste. (2) The fibres which appear to come 
from the glosso-pharyngeal do not accompany this nerve up 
to its root, for disease of the glosso-pharyngeal root does not 
affect taste ; they may, perhaps, ascend via the tympanic 
nerve and small superficial petrosal to the otic ganglion, and 
thence along the third division of the fifth nerve to its root 
(Gowers). It would thus seem that the whole of the fibres 
of taste are gathered together in the (sensory) root of the 
fifth nerve. The cortical centre for taste is in the same 
region as that for smell. 



CHAPTER V. 

SYMPTOMS REFERABLE TO SPECIAL DIS- 
TRICTS (FACE, TONGUE, LIMBS, ETC.). 

ELECTRICAL EXAMINATION. 

We have already bad to allude to the electrical reactions of 
muscles ; and to the present chapter, which will deal chiefly 
with the functions of particular muscles and nerves, we shall 
prefix a short account of the uses of electricity in diagnosis. 
Electrical Examination of Muscles. — We shall confine 
ourselves to its (commonest) use in testing muscles and motor 
nerves, the electrical examination of the special organs being 
a subject too difficult to deal with here. In testing either 
muscle or motor nerve, the effect to be observed, and from 
which conclusions are to be drawn, is the same for both — viz., 
a muscular contraction ; for the condition of the motor nerve 
reveals itself only by its action on the muscle. This effect 
may be produced in two ways, either (i) by the direct appli- 
cation of the current to the muscle, or (2) indirectly by the 
application of it to the motor nerve of the muscle. In health 
the same result is obtained by both methods ; but in disease, 
as we shall see, there may be modifications which show them- 
selves only when galvanism is applied directly to the muscle. 

The Two Kinds of Current and their Effects 
upon Normal Muscle. — Two kinds of current are used 
in testing: (1) the faradic, otherwise called the induced or 
interrupted current; (2) the galvanic, also called the voltaic, 
or continuous, or constant current. The mere passage of a 
galvanic current through a normal nerve or muscle causes no 
stimulation, and therefore no contraction, so long as this 
148 



ELECTRICAL EXAMINATION. 149 

current does not vary in strength ; to elicit a muscular contrac- 
tion its strength must be made to vary rapidly. This is most 
effectually done either by rapidly making the current (closing the 
circuit) or by rapidly breaking it (opening the circuit), which 
causes a sudden rise or fall of current strength from or to zero. 
There is in this respect an important difference between the two 
kinds of current. The faradic current is by its very nature vari- 
able in strength, consisting, as ordinarily applied, either of one 
rapidly appearing and disappearing current (single induction 
shock), or of a succession of such momentary currents. Its 
effect, in health, is to produce a single sharp muscular twitch 
when a single current is passed, a tetanic contraction of 
muscle when a series of such currents is passed. The galvanic 
current, on the other hand (viz., that obtained directly from 
the poles of a series of galvanic cells), when once established 
through the body, flows equably and permanently. During 
the flow of such an equable current effects indeed are produced, 
but no stimulation such as can cause muscular contraction. 
When, however, a current of sufficient strength is either made 
or broken, a sharp single muscular contraction follows, just as 
in the case of the single induction (faradic) current. And this 
contraction is, as we have said, the same, whether the appli- 
cation of the current be to the muscle directly or to its motor 
nerve-trunk. Stimulation even more effective than that caused 
by simply making or breaking such a current may be obtained 
by rapidly reversing its direction (voltaic alternative).* 



* A T ote on Apparatus. — A faradic battery consists of the following parts : 
One or two good-sized cells, the current from which circulates through a 
coil of (comparatively) stout wire, called the primary coil. Encircling this 
coil, but not in connection with it, is placed another coil of finer wire, 
called the secondary coil. The circulation of the current in the primary 
coil, when flowing equably, produces no effect in the secondary; but when 
the primary current is rapidly made or broken, a current of considerable 
electro-motive force but of extremely short duration appears in the sec- 
ondary coil. This is the current which supplies the " single induction 

x 3 



I50 NERVOUS DISEASES. 

Localization of Current. — But before considering this 
contraction further, we must explain in what sense a current 
which in reality circulates through the whole body can be 
said to be applied to a particular part of it, such as a muscle 
or nerve. The explanation will apply to either current, fara- 

shock " and causes a single muscle-twitch. An automatic hammer (which 
we need not describe fully) is attached to the apparatus, by which the cur- 
rent in the primary coil is continuously made and broken, and thus a series 
of induced currents (or, as it is shortly called, a faradic current) is set up 
in the secondary coil. This series of shocks produces tetanus of the mus- 
cle. The strength of this current is graduated either by sliding the second- 
ary coil more or less over the primary, or by sliding between the coils a 
metal tube which serves to shield one from the other. The distinction of 
poles, so important to observe in the galvanic apparatus, is of less conse- 
quence in the faradic. In most batteries provision is made for using either 
the currents in the secondary coil or those in the primary. The secondary 
currents are as a whole the strongest and the most acutely felt, and most 
suitable for stimulating the skin and its sensory nerves; the primary are 
milder, and perhaps the best fitted for eliciting contraction of deeper- 
seated muscle. 

K galvanic battery consists of a number (about 40) of cells connected 
in series— i.e., the negative pole (zinc) of one connected to the positive 
pole (carbon) of the next. The object of this is to provide a sufficient 
electro-motive force to overcome the resistance of the skin, which is very 
large. The current obtained will be directly proportional to the electro- 
motive force {i.e., roughly speaking, to the number of the cells used), and 
inversely proportional to the resistance. Since this resistance varies 
according as the skin is moist or dry, or according to the part of the body 
tested, it evidently contributes a very important factor toward the strength 
of the current, quite as important as the number of cells used. Thus if 20 
cells, each giving 1^ volt electro-motive force, are applied through a part 
where the resistance is comparatively high, say 3000 ohms, then the cur- 
rent strength will be jf^ amperes or 10 mille-amperes, a strong but bear- 
able current. The same cells applied through a part when the resistance 
is low, such as the face, would give, reckoning the resistance as 1000 
ohms, a current of 30 mille-amperes, unbearable to most patients. The 
galvanic current is usually graduated by a dial or sledge which admits of 
any number of cells being thrown into circuit, and thus varying the electro- 
motive force used. (It may also be graduated by a contrivance called a 



ELECTRICAL EXAMINATION. 151 

die or galvanic. From the two poles of the battery the cur- 
rent is conducted by insulated wires, called rheophores, and 
thence into the body by means of metal plates or discs, termed 
electrodes, which are covered with wash-leather and well 
moistened with warm water, so that their moisture may reduce 
the resistance of the skin. The current enters the body at 
the point of application of one electrode, then spreads itself 
out over the internal tissues, and is again gathered up at the 
point of application of the other electrode, where it leaves 
the body (Fig. 46). The two electrodes therefore constitute 
narrow necks in the channel of the current, where it becomes 
concentrated. This concentration, or "density," depends 
on two things : first, the absolute strength of the current 
used, and, secondly, the smallness of its channel at the par- 
ticular point in question (in other words, the density is directly 
proportional to the current strength and inversely propor- 
tional to the area of its section). The effect of the current 
depends on its density ; and it can thus for practical purposes 
be localized at any sufficiently superficial point by using a 
moderately small electrode. 

This fact is utilized in what is called the "unipolar 

rheostat for varying the resistance in the circuit.) The terminals of the 
battery {i.e., the screws to which the rheophores are to be attached) should 
be marked so that it can be seen at once which corresponds to the nega- 
tive and which to the positive pole. There should be also a handle (com- 
mutator) whereby the current can be made or broken, or its direction 
reversed (poles changed) without removing the electrodes from the patient. 
Further, there should be a galvanometer graduated in mille-amperes for 
measuring the current during its passage ; and the needle thereof should 
come to rest quickly (dead-beat) in order to save the time of the operator 
and the skin of the patient. Without a galvanometer the current strength 
can only be guessed at, or measured by its effects, which is obviously 
illogical when its effects are what we wish to test. Rhe phores and elec- 
trodes of proper sizes, and an interrupting handle by which the make and 
break of the current are under the contiol of one finger of the operator, 
complete the requisites for electro-diagnosis. 



152 



NERVOUS DISEASES. 



method" of testing as follows: One of the electrodes, of 
large size, and therefore giving but a slight concentration of 
current, is applied at any point, such as the nape of the neck, 
sternum, buttocks, etc., sufficiently far from the part we wish 
to test. This is called the "indifferent" electrode. The 
other or " different " electrode is of small size, so as to con- 
centrate the current, and is applied over the part to be 
tested. The current is thus concentrated to a maximum at 
this noint, and is said to be localized there. 




Diagram to Illustrate the Concentration of the Current 
Point of Application of the Smaller Electrode. 



JNDB8 THE 



EFFECTS OF DIFFERENT POLES. 

Normal Polar Formula. — The next question, that of 
the different action of the two poles, is of importance only 
with reference to the galvanic current, and may practically 
be neglected with respect to faradism. That electrode which 
is connected to the negative pole (or zinc element) of the bat- 
tery is called the kathode (and designated by the symbol K) ; 
the other one which is attached to the positive pole (carbon 



ELECTRICAL EXAMINATION. I 53 

element) is called the anode (and designated by the symbol A). 
There is a difference in the readiness of the muscular response, 
according as (i) the kathode or anode is placed on the part 
to be tested, (2) the current is made or broken. Thus, if we 
take a healthy nerve or muscle, and ascertain by gradually 
raising the current strength what are the minimum strengths 
at which we can obtain contractions with kathode or anode, 
and with make and break respectively, we shall find that they 
fall into the following order: — 

(1) To obtain a contraction with the least current strength, 
the kathode must be placed on the muscle or nerve, and the 
current made (circuit closed). This is designated in symbols 
as follows : — 

K. C. C. 

(Kathode). (Closure). (Contraction). 

or German — 

K. S. Z. 

(Kathode). (Schliessung). (Ziickung). 

(2) With a greater current strength, a contraction may be 
obtained when the anode is on the muscle or nerve, and the 
current is made (circuit closed) ACC or German ASZ. If 
the kathode be substitued for the anode with this current 
strength, its action is greater than that of the anode, KCC 
> ACC. 

(3) With a still greater current strength, the anode causes 
a contraction when the current is broken (circuit opened) ; 
AOC, German AOZ. (This is the general rule ; but some- 
times even with healthy tissues AOC occurs before ACC.) 

(4) Lastly, with a current strength which is to most patients 
unbearable, the kathode causes contraction when the current 
is broken (circuit opened) ; KOC, German KOZ. 

The usual " polar formula " therefore is — 

KCC > ACC > AOC > KOC, 
K or A indicating the character of the " different " electrode ; 
and > that the contraction occurs at a lower current strength, 



154 NERVOUS DISEASES. 

or is greater when produced by the same strength. But there 
may be, as just stated, a little uncertainty as to the order in 
which the anodal closing and opening contractions follow 
each other. (A very slight contraction may be indicated by 
a small c or z.) 

It should further be noted, that in health the character of 
the muscular contraction is a sharp, short twitch, quickly 
evoked and quickly subsiding. 

Motor Points. — If an electrode of moderate size be 
passed over a muscle, it will usually be found that there is 
one point in the skin at which the current most readily calls 
forth contraction. This is called the " motor point" of the 
muscle, and in testing the contractility of the muscles to 
weak currents (at any rate when they still respond to farad- 
ism), we should remember the existence of such points. 
Maps* of the motor points have been prepared, but unfortu- 
nately they differ considerably in different individuals. 

Abnormalities in Electrical Reaction. — The devia- 
tions from the normal electrical reactions, which are observed 
in disease, are of two main kinds : — 

(i) Quantitative, i.e., simple excess or defect in readiness 
of response to the electrical stimulus. 

(2) Qualitative — i.e., changes either in the character of 
the muscular contraction or in the normal polar formula. 

Quantitative variations in electro-irritability are usually 
in the way of defect, but excess of electro-irritability is said 
to occur in tetany and some other conditions. Diminution 
occurs in that form of muscular atrophy wherein the disease 
falls primarily on the muscular tissue, and not on the nerves 
or nerve-centres; in muscular atrophy that is secondary to 
joint disease, and sometimes in peripheral neuritis. We 
should not too hastily conclude that the electro-contractility 
of a muscle is diminished because it appears to react badly. 

* Vide figures at the end of the book. 



ELECTRICAL EXAMINATION. I 55 

A certain allowance must be made for differences between 
different patients and between muscles in different parts of 
the body. Therefore it is well, wherever practicable, to con- 
trast the reaction of a muscle with that of its fellow on the 
opposite side. Again, the apparent defect in reaction may 
be really due to defect in the current used ; either because 
the electro-motive force of the battery is insufficient, or 
because the resistance in the skin of the part is unusually high. 
This fallacy may be avoided by the use of the galvanometer. 
Qualitative changes are, as a rule, elicited by galvanism 
only, and by the direct application of galvanism to the 
muscle. Qualitative changes are evidenced as follows : 
Reaction of Degeneration. — The character of the mus- 
cular twitch alters ; it becomes sluggish, developing and 
subsiding slowly. The polar formula is modified, and usually 
in this sense, that the current strength required to produce 
contraction with anodal closure is not greater, or is even less, 
than that required with kathodal closure (ACC = or > KCC). 
Such changes constitute what is called the reaction of degen- 
eration (RD, or German EaR). When they occur, we gen- 
erally find that at the same time there is loss or great diminu- 
tion of contractility to currents applied in the other way — 
namely, to faradism, whether applied to the nerve or muscle, 
or to galvanism applied to the nerve.* In this case, the 
reaction of degeneration is said to be "complete." If, as 
occasionally happens, qualitative changes are present without 
loss of farado-contractility, the reaction of degeneration is 
" incomplete." 

* The electro-contractility of muscle is probably of two kinds — the 
neuro-muscular, which is produced by the intervention of nervous influence, 
this influence being evoked by the application of faradism to the nerve- 
trunk or nerve-ending, or of galvanism to the nerve-trunk; and the itlio- 
niusculnr, produced by the application of galvanism to the muscle. When 
the neural influences are removed, the idio-muscular phenomena can be 
studied by themselves. 



I56 NERVOUS DISEASES. 

Meaning of the Reaction of Degeneration. — The 

main inference to be drawn from the presence of the reaction 
of degeneration is this : that a degenerative process has been 
set up in the muscle consequent on some interference with the 
trophic influences which are normally exercised upon it by 
the cells of the anterior gray cornua of the cord. Either the 
cells themselves have been injured, or the nerve has suffered 
in some part of its course between the cells and the muscle.* 
Reaction of degeneration is therefore the clinical concomitant 
of Wallerian degeneration {vide p. 77). Along with it are 
generally to be found paralysis and wasting of the muscle, 
but the three factors may be present in very unequal degrees. 
The phenomenon is best watched where the lesion is acute, 
say in an ordinary case of facial paralysis (acute neuritis of 
the facial trunk). For the first few days there is no change 
in electro-irritability. Then the response to faradism, whether 
applied to the nerve-trunk or to the muscles, and the response 
to galvanism as applied to the nerve-trunk {i.e., the neuro- 
muscular electro-contractility), begins to fail, and rapidly 
disappears altogether. Per contra, the response to galvanism, 
as applied to the muscle (idio-muscular electro-contractility), 
is increased, and with this increase appear the characteristic 
phenomena of RD, which we have already described. Roughly 
speaking, about a week is required for the development of 
these changes. After a week or two more, if the disease is 
mild and transitory, the increased galvano-contractility falls 
again, the motor paralysis begins to disappear, the farado- 
contractility reappears, and the qualitative changes return to 
normal. If the case is more severe, the galvano-contractility 
falls even below normal, but neither the motor power nor the 

* As a rule, therefore, RD enables us to localize the lesion, though it is 
true that in some diseases, such as lead paralysis, wherein it occurs we 
cannot confidently assert this. Some recent German observations indicate 
that a modified RD may be present in cerebral lesions; but these observa- 
tions require further confirmation. 



THE FACE. 157 

farado-contractility return, and the qualitative changes persist. 
In the worst cases of all, this state of affairs goes on till the 
galvano-contractility also disappears, so that the muscle is left 
paralyzed, wasted, and without electro-contractility of either 
kind. 

When the disease is not acute, but insidious in onset and 
spreads gradually, the phenomena are less regularly developed. 
The stage of increase in the galvano-contractility may be 
absent. The failure of farado-contractility in some fibres 
may be masked by reason of its retention in neighboring 
fibres, and care may be required to demonstrate the qualitative 
changes. Probably these will become evident enough as the 
disease progresses. Just as in acute lesions the motor power 
returns before the electrical abnormalities disappear, so in 
chronic and widespread disorders we may find electrical 
changes in muscles which were not known to be paralyzed ; 
for the presence of RD indicates, as we have already said, a 
defect of nutrition rather than a paralyzing lesion, though the 
latter is usually associated with it. 

THE FACE. 

Paralysis from Disease of Facial Nerve-Trunk. — 

Facial paralysis, when due to disease of the facial nerve-trunk, 
is almost always unilateral. It involves all the muscles of one 
side, those of the forehead and the orbicularis oculi, as well 
as the lower facial muscles. This distinguishes it from the 
facial paralysis caused by disease of one cerebral hemisphere, 
wherein the muscles of the forehead and the orbicularis oculi 
for the most part escape. The affected side of the face is 
motionless and expressionless, the naso-labial fold is less 
marked than on the sound side, the angle of the mouth gen- 
erally droops. The features may be distorted, being pulled 
over by the muscles of the sound side. The paralysis, if not 
obvious when the face is at rest, becomes so when the muscles 
are thrown into action. Thus, on showing the teeth, the 
14 



I58 NERVOUS DISEASES. 

mouth is drawn over to the sound side. On shutting the 
eyes, the lids of the affected side remain open, while the eye- 
ball rolls upward (concealing the cornea, perhaps, but not the 
whole sclerotic). Owing to continual want of apposition of 
the lower lid, the tears are apt to run from the affected eye. 
On attempting to whistle, the air escapes from the paralyzed 
corner of the mouth. The paralyzed buccinator bulges when 
the mouth is inflated ; and during mastication it lets the food 
slip between the gums and the cheek. If the muscles be 
tested electrically, reaction of degeneration will be found (in 
all but the mildest cases) after the first week of the disease. 

There are two common causes for such a facial paralysis : 
(1) exposure to cold, as from sitting at an open railway- 
carriage window, sleeping in a draught, etc. ; this is called 
"rheumatic neuritis." 

(2) Suppurative disease of the middle ear, especially when 
accompanied with bone-disease. The course of the nerve 
through the inner wall of the tympanum renders it liable to 
inflammatory change from this source. Further, syphilis is 
alleged to be a cause of facial neuritis, and facial paralysis 
may be associated with paralysis of other cranial nerves in 
tumors, injuries and disease of bones, etc., affecting the base 
of the skull. 

The onset of a facial paralysis is generally acute. At the 
commencement of a " rheumatic " case there may be pain in 
the side of the face ; this is said to be due to a coincident 
affection of the trigeminus. In a mild case the paralysis may 
subside in the course of a few weeks. Electrical examination 
may prove useful in prognosis ; for if (in a case known to be 
due to disease of the nerve-trunk) the electrical reactions are 
normal after a week or fortnight, the case is a mild one, and 
will probably recover soon. But severer cases may last for 
months, and some may prove quite irremediable. In long- 
standing cases the muscles degenerate and shorten, so that the 
face appears drawn to the paralyzed side. But this is only 



THE FACE. 159 

when at rest ; on making the patient shut his eyes, etc., it will 
be quite obvious which side is paralyzed. 

In the early stages, counter-irritation, in the shape of a 
blister, may be applied over the nerve-trunk. Iodide of 
potassium may be administered. The ear should always be 
examined, and treated if active disease exist in it. After the 
first ten days, electricity may be applied to the muscles ; 
galvanism is usually required, because they no longer act to 
faradism. The eye, being unprotected by closure of the lids, 
is apt to become inflamed, and therefore it should be care- 
fully protected from wind and dust. 

In some cases of facial paralysis there is loss of taste on the 
corresponding side of the tongue. This means either (1) that 
the facial nerve-trunk is diseased in that part of its course 
where it contains the fibres from the chorda tympani — i. e., 
between the geniculate ganglion above and the origin of the 
chorda (at the lower part of the aqueductus Fallopii below) ; 
or (2) that the chorda tympani is involved simultaneously, as 
may well happen in disease of the ear. 

Again, it has been stated that in disease of the facial nerve 
above the geniculate ganglion the corresponding half of the 
soft palate and uvula is paralyzed, since the motor fibres 
to those parts run, via the facial root and geniculate ganglion, 
through the large superficial petrosal nerve to Meckel's gang- 
lion, which latter ganglion supplies the soft palate. But the 
clinical fact appears to be doubtful. 

Double facial paralysis (from disease of the nerve-trunks) is 
a rare occurrence. Some constitutional cause (such as syph- 
ilid is here more likely than in unilateral disease. Bilateral 
ear-disease may also cause it. The whole face is like a mask : 
the patient may weep bitterly, or be convulsed with laughter, 
but his facial muscles betray no emotion. 

Other Causes of Facial Paralysis. — Facial paralysis 
may be caused not by disease of the nerve-trunk, but by a 
central lesion, affecting either (1) the nerve-nucleus in the 



l60 NERVOUS DISEASES. 

pons, or (2) the parts above this — viz., the cerebral cortex or 
motor tract between the cortex and nerve-nucleus. In (1) 
"nuclear" paralysis, the facial palsy is probably more limit- 
ed than in disease of the nerve-trunk.* And there may be 
further symptoms indicating disease of the pons, either para- 
lysis of other cranial nerves or cross paralysis. 

In (2) "supra-nuclear" paralysis we look for traces of 
hemiplegia on the same side ; but even in the absence of this 
we may distinguish as follows. Facial paralysis, when the 
lesion is in the cerebral hemisphere, does not affect the orbi- 
cularis oculi, or occipito-frontalis, so that the patient can still 
frown and close his eye. Secondly, the electrical reactions 
in such a case are not altered. 

Lastly, the facial muscles may be affected in some forms of 
progressive muscular atrophy (infantile myopathy), but such 
affection is bilateral. 

Facial Spasm. — Muscular spasm in the district of the 
facial nerve (motor tic) is far less common than paralysis. 
It mostly occurs as paroxysms of clonic spasm, affecting more 
particularly the orbicularis oculi and zygomatici. Unlike 
facial palsy, it begins gradually ; it may last a very long time. 
It may be due to direct irritation of the facial trunk (from 
tumor, aneurism, or the like), or reflexly to irritation of the 
trigeminus (decayed teeth, etc.), or to disease of the cerebral 
cortex. Such conditions as mental anxiety, grief, etc., often 
precede it. 

Facial Neuralgia. — The sensory nerve-supply of the 
head and face is represented in Fig. 47. The face, with the 
exception of the skin near the parotid and lower jaw, is sup- 

* It seems probable, from the facts of glosso-labio-laryngeal palsy (vide 
infra, p. 163) that the motor supply of the lips comes from the hypoglos- 
sal nucleus, and not from the facial. It is also thought that the orbicularis 
oculi is innervated from the third nucleus. Thus the facial nucleus proper 
would innervate only the lower part of the face, and that with the excep- 
tion of the orbicularis oris. 



THE FACE. l6l 

plied by the three branches of the fifth nerve ; the back of 
the head by the great occipital (posterior division of second 
cervical nerve), the remaining parts from the cervical plexus 
(small occipital, great auricular, and superficial cervical 
nerves). The most important sensory affection of these parts 
is facial neuralgia. Evidently the fifth nerve is specially 
obnoxious to two common causes of neuralgia, (i) exposure 
to cold, (2) peripheral irritation, since it is the sensory nerve 




supra - 



nasal. 
l.K 



Diagram of the Cutaneous Nerve-Supply of the Face and Head. {After 
Flower. ) 



of the teeth. Again, since it passes through bony foramina, 
it may be easily affected by swelling of its sheath, or of the 
periosteum in its neighborhood. Malarial neuralgia is a 
form which specially affects the supra-orbital division ; it is 
known as brow-ague. The so-called epileptiform neuralgia 
is characterized by the extreme suddenness and violence of 
the pain. The points of emergence of the fifth nerve upon 
the face should be noted. The pains are apt to radiate from 
them, and they are often specially tender to pressure. 



1 62 NERVOUS DISEASES. 

" Cervico-occipital " neuralgia is less common than facial. 
Both this region and that of the face may be selected by the 
lightning pains of tabes dorsalis. 

Hemiatrophy of Face. — The curious disease known as 
"facial hemiatrophy" is possibly due to disease of the fifth 
nerve. In this disease the skin, subcutaneous tissue, hair, 
bones, in short all the tissues except the muscles, waste gradu- 
ally, but only upon one side, so that the patient's face appears 
to be made up of two dissimilar halves, one smaller than the 
other and wizened-looking. Sometimes a thin furrow divides 
the two. There is, however, no affection of sensibility, and 
the electrical reactions of the muscles are normal. Sometimes 
there is wasting of the skin or bones of other parts of the 
body. 

THE TONGUE. 

Paralysis and Atrophy of the Tongue. — The motor 
nerve of the tongue is the hypoglossal ; the lingual branch of 
the fifth supplies it with common sensibility ; of the sense of 
taste we have already spoken. 

Paralysis of the tongue, like that of the face, may result from 
disease of the motor nerve-trunk, of its nucleus, or of the parts 
above. Paralysis of one-half the tongue usually indicates 
disease of the nerve-trunk, or of the opposite cerebral hemi- 
sphere ; in the first case the paralysis is accompanied by 
wasting, in the second case it is not. In either case the tongue, 
when protruded, deviates toward the paralyzed side, since 
the tongue is under normal conditions pushed out, and 
in unilateral paralysis the unbalanced action of the healthy 
muscles push it over. Such unilateral paralysis interferes 
little with the functions of the tongue. Bilateral paralysis is 
usually nuclear in origin. In such a case the tongue wastes, 
becoming thin, flabby, and wrinkled longitudinally. It can 
only be protruded imperfectly, or not at all. Difficulty in 
articulation and, still more, difficulty in swallowing, are the 
chief symptoms. Such wasting palsy of the tongue commonly 



THE PALATE AND LARYNX. 1 63 

forms part of a more general muscular atrophy (progressive 
bulbar paralysis), but it may be the earliest symptom thereof. 
With it may be associated paralysis of the lips, palate, and 
larynx. 

It would appear that in exceptional instances unilateral 
palsy of the tongue may be due to nuclear disease ; such appears 
to be the case when hemiatrophy of the tongue occurs in tabes 
dorsalis, or in general paralysis. Conversely, bilateral palsy 
may be due to disease of the hemispheres, either when the 
cerebral disease is bilateral, or sometimes even when it is 
unilateral. 

The Palate. — The natural movement of the palate is best 
seen by making the patient open his mouth, and say " ah " 
or "eh," drawing in his breath the while. (The tongue is to 
be kept depressed by a spatula, if necessary). The palate is 
then drawn upward in the form of a symmetrical arch. If the 
whole palate is paralyzed, the whole of it hangs motionless. If 
one side is paralyzed, the palate moves, but not symmetrically. 
The upward traction takes place from the centre of the sound 
side, and therefore causes the sound side to rise highest, and at 
the same time to become " dimpled." Palatal paralysis is 
common as a sequela of diphtheria; the whole palate is affected, 
the voice becomes nasal, fluids while being swallowed are apt 
to regurgitate through the nose. It occurs also in progressive 
bulbar paralysis. In this disease, as above remarked, there is en- 
grafted upon paralysis of the tongue paralysis of the lips, palate, 
and larynx. That of the tongue, and probably of the lips, 
is caused by disease of the hypoglossal nuclei ; that of the 
larynx, and probably of the palate, to disease of the adjacent 
spinal accessory nucleus. Similarly, unilateral paralysis of the 
tongue, palate, and larynx has been seen in disease involving 
the roots of these two nerves upon one side of the medulla. 

Paralysis of the Larynx. — The intrinsic muscles of 
the larynx are supplied by the recurrent laryngeal nerve. 
This nerve, though it branches from the vagus, is probably 



164 NERVOUS DISEASES. 

ultimately derived from the spinal accessory. For clinical 
purposes, we may divide the muscles of the larynx into two 
groups: (1) adductors (and tensors), which approximate the 
two vocal cords, and which are necessary for phonation ; (2) 
abductors, which separate the cords, and therefore are neces- 
sary for respiration. When one vocal cord is paralyzed com- 
pletely {i.e., both as regards abduction and adduction) (Fig. 

Fig. 48. 



JE 



Complete Paralysis of Left Vocal Cord (Paralysis of Recurrent Laryn- 
geal Nerve); Position of Cords During Inspiration. (After Ziemmsen.) 

48), it stands on a slightly different level to its comrade, and 
midway between the positions of complete abduction and 
complete adduction. This is called the cadaveric position, 
since it is that which the cords assume post-mortem. During 
deep inspiration it is not abducted, nay, the entering current 
of air may even make it flap inward slightly. During phona- 

Fig. 49. 



Ml 




Complete Paralysis of Both Vocal Cords (Cadaveric Position of Cords). 
(After Ziemmsen.) 

tion it is not adducted, but the sound cord may cross the 
middle line to meet it, thereby rendering phonation just pos- 
sible. But the voice is apt to be hoarse, and the cough inef- 
fective. Such a condition points to disease of one recurrent 
laryngeal nerve, the ultimate source of which is often to be 
found within the chest — viz., pressure upon or destruction of 



THE LARYNX. 1 65 

the nerve from a new growth, or aneurism. An aneurism is 
particularly probable if the paralysis is left-sided ; because the 
left recurrent nerve winds round the arch of the aorta. 

Complete paralysis of both cords (Fig. 49) is a very rare 
condition : here the voice is whispering, coughing is im- 
possible ; respiration is normal, save that the patient may be 

Fig. 50. 



#> 



Bilateral Paralysis of Posterior Crico-Aryt^noids (Abductor Paralysis) ; 
Position of Cords During Inspiration. (After Ziemmsen) 

unable to husband his breath sufficiently to say a long sen- 
tence or make a prolonged effort without taking breath. 

Abductor paralysis (Fig. 50) is bilateral as a rule. The 
two cords stand near the middle line ; during inspiration they 
do not move outward (they may even flap inward a little), but 
in phonation they act normally. The voice is unaffected, the 




Bilateral Paralysis of Internal Thyroarytenoids; Position of Cords 

Xfter Ziemmsen.) The 

[ysterical Aphonia.) 



During Phonation. (After Ziemmsen.) The Usual Condition in 
Hys 



cough is natural. As to respiration, in mild cases little more 
may be noticed than that inspiration is long and wheezy. 
But should any further source of obstruction arise, such as a 
laryngeal catarrh, or should the paralysis grow rapidly worse, 
the aperture of the glottis becomes inadequate, inspiratory 
dyspnoea arises, and tracheotomy is required. Such bilateral 
abductor paralysis may occur in various degenerative nervous 



1 66 NERVOUS DISEASES. 

diseases ; particularly in tabes dorsalis, wherein it may be an 
early symptom. It is a remarkable fact that when any organic 
disease progressively invades the nervous apparatus of the 
larynx, whether in the nerve-trunks or the nerve-centres, the 
first result is abductor paralysis ; the cords gradually ap- 
proximate to the middle of the line, and not to the cadaveric 
position. 

Adductor paralysis (Fig. 50) is also bilateral. The cords 
during attempts at phonation either meet imperfectly or are 
insufficiently tense, but in inspiration they move outward 
normally. The voice is whispering, though the cough is 
(often) natural ; the breathing is natural. This condition 
occurs without known organic cause, and constitutes what is 
known as "hysterical aphonia." 

Laryngeal spasm is chiefly seen in the " laryngismus 
stridulus " of rickety children. 

Laryngeal anaesthesia we shall not consider here. For its 
investigation much dexterity with the mirror and sound is 
necessary. 

Anaesthesia of the fauces, or (more strictly) abolition of 
the reflex caused by irritation of the fauces, is usually 
hysterical. 

Respiratory Muscles. — Paralysis of the muscles of respi- 
ration may be considered here. The diaphragm is the prin- 
cipal inspiratory muscle. Its action, according to Duchenne, 
is twofold. First, it draws up the lower ribs, to which it is at- 
tached, and thereby expands the lower part of the chest. 
This it can only do by acting on the convex and partially re- 
sisting surface supplied to it by the liver and spleen. (The 
resistance offered by these organs is conditional on the sup- 
port which they receive from the muscles of the anterior ab- 
dominal wall. Hence, when the abdominal muscles are 
paralyzed, the diaphragm can no longer raise the lower ribs.) 
Seco7idly, it depresses the floor of the thorax, thereby increas- 
ing the chest capacity. Its contraction makes the floor fiat 



RESPIRATION. 1 67 

instead of dome-like, and drives before it the abdominal 
viscera. The visible effect of this is distention of the epi- 
gastrium during inspiration. 

In paralysis of the diaphragm the expansion of the lower 
part of the chest is deficient, as compared with that of the 
upper, which is worked by the intercostals ; and the epigas- 
trium, instead of rising during inspiration, tends to be sucked 
in. Paralysis of the diaphragm may be caused by disease of 
the cord above the fourth cervical root, from which the 
phrenic nerve mainly originates (in this case the intercostals 
will also be paralyzed) ; from disease of bone or meninges at 
the level of the fourth cervical root ; from disease of the 
phrenic nerves themselves, which may occur in alcoholic 
neuritis, lead poisoning,diphtheritic paralysis, or from aneurism 
or intra-thoracic growth ; in muscular atrophy spreading to 
the diaphragm. Inaction of the diaphragm may be seen in 
some cases of pericarditis or pleurisy. 

As to the intercostal muscles, the bulk of them, at any rate, 
serve as muscles of inspiration. The movement of inspiration 
as performed by the intercostals only consists mainly of expan- 
sion of the upper part of the chest (superior costal type of 
respiration). The action of the intercostals without that of the 
diaphragm may suffice for quiet respiration, but should effort 
be required, or should respiration be embarrassed by the ad- 
vent of any lung affection, dyspncea sets in. Still more critical 
is the condition of the patient if both intercostals and dia- 
phragm have failed, and respiration be left to the extraordi- 
nary muscles of inspiration, sterno-mastoids, trapezii, ser- 
rati, etc. 

Expiration is usually performed by the elastic recoil of the 
lungs ; but for powerful expiratory efforts, as in cough, sneez- 
ing, etc., the muscles of the anterior abdominal wall are 
required, and their paralysis will render such actions impos- 
sible. 



1 68 NERVOUS DISEASES. 

PERIPHERAL AFFECTIONS OF LIMBS AND TRUNK. 

As the distribution of paralysis, anaesthesia, etc., in the 
body generally is of importance, so also is their grouping 
within particular parts. It is particularly important in the 
limbs. Say that a patient comes complaining of inability 
to perform certain movements ; we have to determine whether 
this indicates paralysis of a particular muscle or muscles ; 
whether the combination of muscles affected corresponds to 
any particular nerve-trunk, or whether it points to central dis- 
ease. 

To fix on the muscles at fault, we must evidently have some 
knowledge of the muscular mechanism of movements ; though 
of course we may be helped in many instances by the appear- 
ance of muscular wasting, and by the results of electrical 
examination. 

We shall therefore consider here the method by which the 
various movements of the limbs are produced in health, 
taking as the basis of our account the writings of Duchenne 
(" Physiologie des Mouvements "). 

Muscular Mechanism of Upper Limb. — The move- 
ments of the upper arm are effected partly at the shoulder- 
joint, partly by movements of the scapula. 

Elevation of the arm, when hanging by the side, is effected 
by the deltoid. Contracting as a whole this muscle lifts the 
arm upward and outward to the horizontal position. But for 
this, support of the scapula is necessary ; such support is 
mainly given by the serratus magnus, which begins to contract 
in association with the deltoid. Contraction of the anterior, 
middle, or posterior parts of the deltoid carry the raised arm 
forward, straight outward, or backward respectively ; and 
their successive action will give it a horizontal sweep as in 
swimming. In the forward movement, the clavicular part of 
the pectoralis major associates itself with the anterior part of 
the deltoid. The supra-spinatus co-operates, though feebly, 
with the deltoid in raising the arm. The posterior part of 



THE UPPER LIMB. IO9 

the deltoid can only lift the arm to an angle of 45 with the 
trunk, and no part of the muscle beyond an angle of 90 (hori- 
zontal position). All further elevation, as in the action of 
lifting the arm above the head, is effected by an upward tilting 
of the acromial end of the scapula. Continued action of the 
serratus magnus, assisted by the upper and outer fibres of the 
trapezius, produces this tilting movement. Paralysis of the 
deltoid is easily recognized : the patient, in endeavoring to 
raise his arm, lifts the point of his shoulder and inclines his 
trunk to the opposite side, but still he cannot separate the arm 
from the side, nor maintain it in the raised position when 
raised for him. Atrophy of the muscle produces flattening 
under the acromion instead of the rounded sweep of muscle 
normally seen there. Paralysis may attack the different parts 
of the muscle separately ; that of the anterior fibres causes 
difficulty in bringing the hand to the mouth, taking the hat 
off, etc.; that of the posterior part, difficulty in buttoning 
the braces behind, in putting the hands into the trouser- 
pockets, etc. Paralysis of the middle fibres may be imper- 
fectly compensated for by combined action of the other two 
parts. 

Depression of the raised arm may be effected by the weight 
of the limb alone, but when force is required the pectoralis 
major and latissimus dorsi are used. The pectoralis major 
acting as a whole brings the arm downward and forward ; 
after the arm has reached the horizontal position the sternal 
fibres still continue to depress it, and finally bring it into ap- 
position with the front of the chest. A forcible downward 
sweep, as in delivery of a sword-cut, is thus produced. But 
the clavicular fibres, after the arm has reached the horizontal, 
no longer depress it, but carry it forward to the middle line. 
The strength of these clavicular fibres may be tested by 
making the patient press together the hands when they are 
outstretched horizontally in front of him ; that of the sternal 
fibres by making him press them together when they are at a 



I/O NERVOUS DISEASES. 

lower level. When the arms hang by the sides, the clavicular 
fibres act as follows : they raise the points of the shoulders 
and bring them round toward the front of the chest, pro- 
ducing the position assumed in crouching, shivering, etc. The 
latissimus dorsi also depresses the arm, but simultaneously 
carries it backward. In so doing it lowers the point of the 
shoulder and carries the whole scapula backward toward the 
spine. Both muscles acting together from the small of the 
back extend the upper part of the spine upon the lower, and 
this with the backward and downward movement of the 
scapulas produces a military carriage. Another muscle — viz., 
the teres major — depresses the arm and carries it backward ; 
but this it can only do when the scapula is fixed (by the 
rhomboids). When the arm is fixed (as by approximation to 
the side of the trunk) the teres major, using it as a fixed point, 
shrugs the shoulder by dragging up the scapula and tilting 
upward its acromial angle. 

All the depressors of the arm, when the raised arm is made 
their fixed point, tend to drag the body upward ; and they 
are thus the muscles used in climbing. 

Rotation of the arm in an inward direction is effected by 
the subscapularis ; in an outward, by the infra-spinatus and 
teres minor. These rotatory movements, according to Du- 
chenne, may supplement the movements of pronation and 
supination in the forearm. The same author notes the curi- 
ous fact that paralysis of the infra-spinatus causes difficulty in 
writing ; the hand can no longer be carried, by external 
rotation of the shoulder-joint, horizontally along the paper 
from left to right. 

Certain muscles appear to act as ligaments of the shoulder- 
joint ; these are the supra-spinatus, long head of the biceps, 
of the triceps, and the coraco-brachialis. We may add the 
muscular fibres contained in the capsule itself. 

Movements of the scapula, which, as we have said, are inti- 
mately associated with movements at the shoulder-joint, are 



THE UPPER LIMB. IJ\ 

of two kinds — viz., a sliding of the whole bone over the sur- 
fece of the chest, or tilting (rotatory) movements which alter 
the relative level of its three angles. The forces which mainly 
serve to hold the bone in balance are, the trapezius, the ser- 
ratus magnus, the rhomboids, and levator anguli, the weight 
of the upper limb, and the action of its depressor muscles. 
The trapezius, at any rate those fibres that run downward and 
outward to the acromial angle of the scapula, tilt this angle 
upward, thereby giving a contemptuous shrug to the shoulder ; 
the other fibres mainly draw the scapula backward toward the 
spine. Forcible lifting of the shoulder, as in carrying a 
burden upon it, is effected, as we have already said, by the 
serratus magnus, trapezius, teres major, clavicular part of pec- 
toralis major. Weakness of the trapezii allows the shoulder 
to droop downward and forward, giving the patient a long- 
necked, round-shouldered appearance. When the trapezius 
and serratus are both paralyzed, the point of the shoulder 
drops markedly, while the lower angle rises and approaches 
the spine ; the bone appears as if it were suspended by its 
inner angle (to which the levator anguli is attached). The 
serratus magnus not only lifts the acromial angle, but moves 
the whole scapula round the chest away from the spine toward 
the front, at the same time keeping the vertebral border 
closely applied to the chest. It is used in forcible forward 
extension of the arm, as in striking out from the shoulder, or 
pushing a heavy weight in front of one. Paralysis of this 
muscle (at any rate when the deltoid is intact) is character- 
ized thus (Fig. 52) : If the patient extends his arm before him, 
the vertebral border of the scapula becomes separated from 
the chest and projects like a wing. The apex of the wing is 
formed by the lower angle tilted upward and away from the 
chest. The rhomboids draw the scapula toward the spine, 
lifting it upward, but tilting it in the opposite way to the 
serratus and trapezius — viz., the acromion downward, the 
lower angle upward and toward the spine. Combined with 



[72 



NERVOUS DISEASES. 



the trapezius and levator anguli, they lift the scapulae upward 
and carry them toward the spine ; the position is that of tug- 
ging backward against a weight. Since they tend to move 
the scapulas in the opposite sense to the serrati, they are used 
to fix these bones when the serrati act on the chest in forced 
inspiration. Further, they fix the scapula for the teres major, 
when it acts as a depressor of the arm. 



Fig. 52. 




Paralysis of Right Serratus Magnus. {From Duchenne.) 

Movements of the Forearm. — Extension is effected by the 
lateral heads of the triceps and the anconeus ; simple flexion 
by the brachialis anticus ; flexion with supination by the biceps. 
Further, the supinator longus is a powerful flexor of the fore- 
arm ; its action as regards supination is to bring the forearm 
into a position midway between pronation and supination. 



THE UPPER LIMB. I73 

Simple supination is carried out by the supinator brevis; 
pronation by the pronator teres and pronator quadratus, 
assisted by the flexor carpi radialis. 

Movements of the Wrist. — The extensor carpi radialis brevior 
produces simple extension, the extensor carpi radialis longior 
extension with abduction, the extensor carpi ulnaris exten- 
sion with adduction. These lateral movements of abduction 
and adduction are most free when the wrist is extended, and 
they are produced by the two lateral extensors. As to flexion, 
the palmaris longus flexes the wrist simply ; the flexor carpi 
radialis flexes with slight pronation; the flexor carpi ulnaris 
flexes the wrist, at the same time turning the ulnar border of 
the hand inward toward the palm (as in the action of a violinist 
reaching round to touch the higher parts of the strings with 
the little and third fingers). These flexors do not, like the 
extensors, produce lateral movements of the carpus. 

Movements of Fingers. — The extensor communis digitorum 
extends first the metacarpo-phalangeal joints, and next the 
wrist-joint ; it also gives the fingers a movement of abduc- 
tion from the middle line of the hand. The flexor profundus 
flexes the middle and last phalanges ; the flexor sublimis the 
middle phalanges ; and this they do most powerfully when the 
wrist is in extension. The interossei, assisted by the lum- 
bricals, abduct and adduct the fingers ; but they have also a 
more important action, viz., to flex the metacarpo-phalangeal 
joints, and at the same time extend the phalangeal joints. 
They are required for many delicate movements of the fingers, 
and particularly that of writing. Like the long flexors, they 
require for their proper action a certain amount of extension 
at the wrist-joint. It may be noticed that between the 
opposed movements of extension and flexion in the wrist 
and finger joints there is a very close connection. Thus, when 
the fist is tightly clenched (flexion of fingers) the wrist instinct- 
ively starts into extension, so as to put the flexors of the 
fingers into a favorable position for acting. Conversely, in 
x 5 



174 NERVOUS DISEASES. 

extension of the fingers the flexors are engaged to moderate 
and steady the movement. These relations between flexors 
and extensors are illustrated in lead paralysis. Here there is 
paralysis of the extensor longus digitorum, and the wrist and 
fingers fall into a position of flexion (wrist-drop). If the 
proper extensors of the wrist be sound, the patient can 
straighten out his wrist when told to do so ; but if he then 
tries to straighten his phalanges the wrist becomes flexed 
again, because action of the flexors normally accompanies 
movements of extension, and therefore occurs during the 
attempt at extension, though the paralyzed extensors remain 
inactive. Again, if the patient's grip be tested, it will be 




Incomplete Paralysis of the Interossei, after Injury to the Ulnar Nerve. 
{After Duchenne.) 

found weak, not because the paralysis extends to the flexors, 
but because these muscles are, through the wrist-drop, unfavor- 
ably placed for action. Again, the patient cannot extend the 
two distal phalanges; this is not because the interossei are 
paralyzed, but because they also cannot act well while the 
hand is in flexion. 

Paralysis of the interossei causes a characteristic pose of 
the fingers ; the last two joints are flexed by the unopposed 
action of the long -flexors, the first joint over-extended by 
that of the extensor communis digitorum, and probably the 
fingers will be awkwardly separated from each other. In its 
early stages (Fig. 53) this condition is most noticeable when 



THE UPPER LIMB. 1 75 

the hands are being used for such purposes as buttoning 
clothes, etc. In complete interosseal paralysis with atrophy, 
particularly when associated with atrophy of the thumb- 
muscles, the hand takes the shape of a claw, "main en 
griffe " (Fig. 54). 

Fig. 54. 




" Main en Griffe," Resulting from Paralysis and Wasting of the Interossei 
Thenar, and Hypothenar Muscles. (After Duchenne.) 

Movements of the Thumb. — The movements of extension 
and flexion are arranged upon much the same plan as in the 
fingers. Thus, the abductor brevis and flexor brevis flex the 
first joint and straighten the second, therein corresponding to 
the interossei. The extensor primi internodii straightens the 

Fig. 55- 




Atrophy of Muscles of Thumb-ball; the Thumb is Drawn Backward into 
the Plane of the Hand, and -Rotated Outward. (After Duchenne.) 

first joint only, corresponding to the extensor communis 
digitorum. The long flexor flexes the second joint. Move- 
ments of abduction and adduction are much more extensive 
than in the fingers. The extensor ossis metacarpi pollicis is 
primarily an abductor of this bone ; secondarily, it abducts 



1/6 NERVOUS DISEASES. 

(draws over to the radial side) the whole carpus, this second 
action being checked by the extensor carpi ulnaris. Adduc- 
tion of the thumb is of two kinds : the first kind is effected by 
the extensor secundi internodii ; not only is the thumb 
approximated to the radial side of the forefinger, but it is 
brought back into the plane of the hand and rotated outward, 
so that it looks in the same direction as the fingers instead of 
partially facing them. The thumb assumes this position when 
the muscles of the thumb-ball are atrophied (Fig. 55). The 
resulting deformity has been compared to an ape's hand. 
The second kind of adduction is produced by the adductor 
and inner half of the flexor brevis ; the thumb is approximated 
to the first finger, but remains in front of the plane of the 
hand. The important movements of opposition are performed 
by the opponens, abductor brevis, and outer head of flexor 
brevis. The opponens turns the metacarpal bone inward 
toward the palm, the other two muscles rotate the first phalanx 
inward, so that the thumb looks toward the fingers, and incline 
the first phalanx, so that the pulp of the thumb can touch any 
finger from the first to the little finger. 

It is worth while to notice particularly the movements of 
the thumb and fingers in writing. The thumb is placed in 
partial opposition, and its metacarpal bone slightly abducted ; 
the pen is thus held between it and the two first fingers ; the 
position of the finger-joints being that given by the interossei — 
viz., flexion of the first phalanx and extension of the distal 
phalanges. The down-stroke is then made by the action — 
upon the fingers, of their long extensors and flexors, which 
bend the distal phalanges and partially straighten the first 
phalanx — upon the thumb, of its long flexor, which bends the 
second phalanx, and of the extensor primi internodii, which 
straightens the first. Next, the up-stroke is made by the 
interossei, which extend the last two phalanges and slightly 
flex the first, while the abductor brevis performs the same 
office for the thumb. The whole hand is carried along the 



THE UPPER LIMB. 



177 



line as it writes by an external rotation of the shoulder, 
effected by the infra-spinatus. 

Defects Due to Paralysis, etc., of Special Nerves 
of Upper Arm.— When paralysis can be referred to par- 



Musculo-spiral (external 
spiral branch). 



Musculocutaneous. 




Cervical plexus 

(descending branches). 



lntercosto-humeral. 



Lesser internal cutaneous 
(nerve of Wrisberg). 



Internal cutaneous. 



Diagram of Cutaneous Nerve-Supply op Upper Limb. {After Flower.) 
A. — Anterior Surface. 



ticular muscles, the next step is to see whether the muscles 
affected can be grouped under any one nerve. This and the 
corresponding delimitation of sensory paralysis is evidently a 
matter to be determined from anatomical knowledge. For 



7 8 



NERVOUS DISEASES. 



details we must refer the reader to anatomical text-books, but 
we append some diagrams (Figs. 56 and 57) indicating the 
nerve-supply of the skin, and a table of the nerve-supply of 
muscles. 



Intercosto-humeral 



Cervical plexus 

(descending branches). 



Lesser internal cutaneous 
(nerve of Wrisberg). 



cutaneous. 




Internal cutaneous branch. 
External cutaneous 

branch of musculo-spiral. 



M usculo-cutaneous. 



-Posterior Surface. 



The sensory nerve-supply in the upper limb is, broadly 
speaking, as follows : — 

In the Hand. — The palm and palmar aspect of the fingers 
and thumb are shared between the median and ulnar nerves, 
the median taking the radial portion, the ulnar nerve the 



THE UPPER LIMB. 1 79 

ulnar portion, and the two districts joining along the middle 
line of the ring-finger. There is an anastomosis of several 
nerves (musculo-cutaneous, median, and radial) on the 
thumb-ball. The dorsum of the hand is similarly shared 
between the radial nerve (branch of the musculo-spiral) and 
the ulnar ; the ulnar having the ulnar part and the radial 
the radial part, their districts meeting along the middle 
line of either the ring or the middle finger. But the dorsum 
of the last phalanx, in those fingers to which the radial goes, 
is supplied not by this nerve but by the median. 

In the Forearm. — The radial part is taken by the musculo- 
cutaneous nerve, the ulnar part by the internal cutaneous. 
Along the front of the forearm these two nerve-districts meet, 
but behind they are separated by a broad stripe which the 
musculo-spiral supplies. 

In the Upper Arm. — The inner aspect is supplied — above, 
by the intercosto-humeral and the lesser internal cutaneous — 
below, by the internal cutaneous. The internal cutaneous 
supplies also most of the front aspect. The external aspect 
is supplied — above (i.e., over the deltoid), by the circumflex — 
below, by the musculo-spiral. The musculo-spiral supplies 
most of the posterior aspect. 



TABLE OF MUSCULAR DISTRIBUTION OF NERVES, IN NECK 
AND UPPER LIMBS. 

Spinal accessory is distributed to Sterno-mastoid. 

Trapezius. 
2d cervical nerve " Sterno-mastoid. 

3d and 4th do Trapezius. 

Levator anguli. 
Scalenus medius. 
Phrenic (mainly from 4th cer- 
vical! " Diaphragm. 
Branch from 5th cervical . " Rhomboids, levator anguli. 
Posterior thoracic (from 5th 

and 6th cervical) " Serratus magnus. 

Branch from trunk* formed by 
5th and 6th cervical " Subclavius. 

1 nerve " Supra- and infra-spinatus. 

Anterior thoracic nerves " Pectoralis major and minor. 



* For further remarks as to the trunk from 5th and 6th cervical roots, 
see p. 181, " Erb's Paralysis." 



i8o 



NERVOUS DISEASES. 



TABLE OF MUSCULAR DISTRIBUTION OF NERVES.— Continued. 



M usculo-cutaneous 
Subscapular nerves 



Circumflex 
Musculo-spiral 



partly.) 

by posterior 

• interosseous 

branch. 



profundus 



is distributed to Biceps, brachialis anticus, co 

raco-brachialis. 
" Subscapularis, lali 

teres major. 
" Deltoid, teres min 

Triceps, anconeus 
Supinator longus 

pi radialis. 
(Brachialis antic 
Supinator brevis 
Extensor carpi I 

ulnaris I 

All the extensors I 

of thumb and 

fingers. J 

Flexor carpi ulnaris 
Ulnar half of flexor 

digitorum. 
Palmaris brevis. 
Interossei and two inner lum- 

bricales. 
Short muscles of little finger. 
Adductor and inner head ot 

flexor brevis pollicis. 
Pronator radii teres, flexor car- 
pi radialis. 
Palmaris longus, flexor sub- 

limis digitorum. 

Pronator quadratus, radial half 
of flexor profundus digitorum. 

Opponens, abductor brevis, 
and outer head of flexor 
brevis pollicis. 

Two radial lumbricales. 



The musculo-spiral trunk is accessible to pressure and to 
electrization in the musculo-spiral groove, between the biceps 
and the supinator longus. It may be difficult to pick out 
here by electrical currents, owing to the violent contraction 
of the neighboring muscles. This nerve is frequently affected 
by pressure, as in the paralysis which results from sleeping on 
the arm or from the use of a badly-made crutch. Extensor 
paralysis results with wrist-drop resembling in some degree 
that of lead palsy. But it is unilateral, and involves the 
supinator longus as well as the extensor of the fingers. 

The ulnar nerve can be felt above and behind the internal 
condyle. It can be stimulated electrically either here or at 
the wrist-joint, just outside the tendon of the flexor carpi 
ulnaris. Ulnar neuritis is by no means uncommon, and one 



THE UPPER LIMB. l8l 

striking result of it is paralysis of the interossei. (Since these 
muscles also fail at the commencement of progressive muscular 
atrophy, careful consideration must be paid to the mode of 
onset, the presence or absence of sensory symptoms, the con- 
dition of the muscles in the other hand, etc.) The median 
nerve can be felt in the upper arm, and stimulated there or at 
the wrist, inside the tendon of the flexor carpi radialis. When 
the median nerve is paralyzed, pronation of the forearm is 
interfered with, and also flexion of the first and second fingers. 
The wrist when flexed deviates to the ulnar side. The move- 
ments of opposition in the thumb are lost and the thumb- 
ball wastes. 

Disease of the circumflex nerve causes paralysis of the 
deltoid, probably with some anaesthesia of the skin covering 
it. (The deltoid may become weak and wasted as a conse- 
quence of disease in the shoulder-joint. But there is then no 
reaction of degeneration and no anaesthesia.) 

Disease of the posterior thoracic nerve causes paralysis of 
the serratus magnus, the main characters of which we have 
already described. 

Affections of Brachial Plexus — " Erb's Paralysis." 
— It is obvious that the distribution of a paralysis will be 
much more complex when more than one nerve-trunk is 
affected, or a cord of the plexus prior to its breaking up into 
nerve-trunks. As an instance of the latter class, we may take 
the following group of symptoms. The deltoid, biceps, and 
brachialis anticus, the spinati muscles, and sometimes the 
supinator longus, are found to be paralyzed. This is believed 
to be due to disease of the trunk formed by the fifth and sixth 
cervical nerve-roots, for, on the one hand, this paralysis has 
been observed to follow injury in the neighborhood of this 
trunk; on the other, faradization of it will, in a healthy person, 
produce contraction of the above-mentioned muscles. The 
electrode should be applied just outside the sterno-mastoid, a 
little way above the clavicle. (This point is called Erb's 
16 



1 82 NERVOUS DISEASES. 

point, and the group of symptoms Erb's paralysis, or some- 
times combined upper-arm paralysis.) 

THE TRUNK. 

Sensory Affections. — The sensory nerve-supply of the 
trunk is comparatively simple. Between the districts of the 
cervical plexus above and the lumbar plexus below the inter- 
costal nerves run in regular zones. In the thorax each 
intercostal nerve is distributed in the corresponding intercostal 
space. In connection with this distribution we may make the 
following remarks : — 

(i) In a transverse spinal lesion, where sensation is 
annulled in the parts below, we can localize the central lesion 
by observing the level to which the anaesthesia reaches. 

(2) In localized disease of the bones, meninges, etc., of the 
dorsal region, the irritation of the nerve-roots involved 
produces neuralgic pains, hyperesthesia, etc., in their distri- 
bution. Such sensory phenomena have been called "root- 
symptoms; " and they may be an early sign of such disease. 

In disease of the cord itself there may be felt at a level 
corresponding to the upper limit of the disease a painful sense 
of constriction, as if from a band tightly tied round the body. 
This is called "girdle pain." 

(3) Apart from organic disease, neuralgic pains, known as 
"intercostal neuralgia," may occur in the distribution of the 
intercostal nerves. Herpes zoster is a trophic affection of the 
skin also to be connected with them. 

(4) Tender points are often found in neurotic subjects at 
various positions in the course of the intercostals — e.g., above, 
or more frequently under, the mammas, at a few inches 
distance from the spinal column, over the spinal column itself, 
in the inguinal regions, etc. 

The commonest painful affection of the trunk, lumbago, 
can scarcelybe considered in connection with nervous anat- 
omy. 



THE NECK. 183 

THE NECK. 

Contractions of Muscles of Neck, or Wryneck. — 
The muscles which balance the head are liable to fall into a 
state of continuous spasm, known as contracture. Contrac- 
ture of these muscles forms the disease known as torticollis or 
wryneck. Sometimes the deformity can be traced home to 
one muscle. In spasm of one sterno-mastoid, the head is 
inclined forward and toward the affected side, rotated 
toward the opposite side, and the chin at the same time tilted 
upward. In spasm of the trapezius (clavicular portion) the 
inclination is backward and to the affected side, with rota- 
tion toward the opposite side. Contracture of trapezius and 
sterno-mastoid together is common. Spasm of one splenius 
inclines the head backward and toward the affected side. 
Spasm of the deeper muscles may also occur (complexus, 
recti capitis, etc.), and it may then be impossible to say which 
are the muscles engaged. 

Torticollis, as an independent disease, mostly occurs in 
patients of middle age or past it. Often there is a history of 
anxiety or mental trouble, business failures and the like. At 
first the spasms may be slight and intermittent, producing 
troublesome jerking movements of the head to one side. 
Then permanent contracture comes on, and the head is fixed 
in the faulty position. Usually the affection is unilateral, so 
as to produce some sort of rotation, but bilateral spasm, pro- 
ducing, for. instance, constant over-extension of the neck, may 
be seen. 

Paralysis of Muscles of Neck. — Paralysis of these 
muscles is mostly seen in progressive muscular atrophy. 
Paralysis of one sterno-mastoid produces little effect : when 
both are paralyzed the head cannot be brought forward from 
the position of over-extension. Paralysis of the clavicular 
part of the trapezius has also little effect on movement, but 
when it is atrophied the shape of the neck is considerably 
altered. Regarding the position assumed in paralysis of the 



I84 NERVOUS DISEASES. 

muscles which balance the head, we must say the same as we 
shall say about the trunk — viz., that in paralysis of one set of 
muscles, say the flexors, the head does not, as might be 
expected, fall back into extreme extension ; but the patient 
keeps it carefully bent forward so that its weight can be kept 
constantly in equipoise by the non-paralyzed extensors. 

Muscles and the Erect Posture. — The muscles of the 
trunk are important agents in maintaining its natural upright 
posture. Since the weight of the body naturally tends to 
bend the spinal column forward, the erectores spinas of the 
two sides are those upon which most work is thrown. Paraly- 
sis of these muscles is seen in the disease known as pseudo- 
hypertrophic paralysis. When the extensors of the lumbar 
spine are failing, the patient instinctively assumes an attitude 
calculated to carry the centre of gravity backward, so that 
if a tendency to fall arise, such tendency may be in the back- 
ward direction, and consequently under the control of the 
non-paralyzed flexors. His attitude is that of a man carrying 
a heavy tray: the upper part of the trunk is bent backward, 
forming an obtuse angle with the lower part ; the hips are in 
extension ; neither the abdomen nor the buttocks are particu- 
larly prominent. A kind of spurious lordosis is thus produced. 
When the erector muscles are weaker on one side than on the 
other, the spine is instinctively bent toward the weak side, 
with the similar object of throwing the weight on the sound 
muscles. A lateral curvature may be thus produced. When 
the abdominal muscles (J. e., the flexors of the spine) are 
paralyzed, a different type of lordosis results, according to 
Duchenne. The centre of gravity has now to be shifted 
forward. This is done by flexing the pelvis on the hips, but 
at the same time, since a certain counteraction appears to be 
necessary, the lumbar spine is arched backward so that a 
saddle-like depression is produced in the loins, the buttocks 
are prominent, and the abdomen protuberant. 

In standing, various muscles of the lower limbs are called 



THE LOWER LIMB. 1 85 

into action besides those of the trunk. The glutsei medii 
prevent sideward movements of the pelvis ; the hamstring 
muscles, together with the posterior and crucial ligaments of 
the knee-joint, prevent that joint from bending forward ; the 
muscles which pass round the ankle, acting as we shall see at 
very various cross directions, brace up the foot and ankle- 
joint. Not only is the action of such muscles necessary, but 
harmonious action. Hence a patient may be unable to stand, 
not only from muscular paralysis, but also from want of 
muscular co-ordination, as in tabes dorsalis. 

MUSCULAR MECHANISM OF LOWER LIMB. 

We will now consider the muscular mechanism of the 
lower limb. 

Movements at the Hip-Joint. — Extension is performed by 
the hamstring muscles and the glutaeus maximus. In standing 
and walking on the level the action of the hamstrings is 
sufficient to prevent the pelvis inclining forward ; but when, 
in consequence of previous flexion of the hip joint, stronger 
extension is needed, as in rising from the sitting or kneeling 
posture, walking up stairs, jumping, running, dancing, etc., 
the glutaei maximi are called into action. This can be appre- 
ciated by palpating the muscles («) while walking on the 
level, (,S) while walking up stairs. The flexors of the hip are 
(1) the iliaco-psoas, which flexes powerfully and at the same 
time rotates the thigh outward, (2) the tensor fasciae femoris, 
which flexes feebly and rotates it inward. Their combined 
action produces simple flexion, but, unless the tensor fas- 
ciae co-operates, the foot is apt to turn out awkwardly. 
Complete paralysis of the flexors of the thigh destroys all 
power of walking, the limb cannot be swung forward nor 
raised from the ground ; mere weakness of them interferes 
with such actions as walking up stairs, where extra flexion is 
required. There are many external rotators (viz., pyramidalis, 



1 86 NERVOUS DISEASES. 

gemelli, obturators, quadratus femoris,* most of the adductor 
muscles, ilio-psoas), as against a few internal rotators — viz., 
the anterior part of the glutseus medius, the tensor fasciae 
femoris, lower part of the adductor magnus. 

The adductor group is numerous and powerful ; one of 
them — viz., the pectineus — is also a flexor of the thigh on the 
pelvis, so that its action (assisted by the ilio-psoas) is repre- 
sented by the movement of crossing one knee over the other 
while sitting. Most of the adductors are also external rota- 
tors, but the lower part of the adductor magnus rotates the 
thigh inward as it adducts it. This is the movement by 
which the rider grips' his horse's flank. 

The glutaeus medius acts differently according to the differ- 
ent parts of the muscle engaged. The anterior part carries 
the thigh forward and outward, at the same time giving it an 
internal rotation ; the middle part simply carries it outward 
(abducts) ; the posterior part carries it backward and outward, 
rotating it outward ; broadly speaking, it is an abductor of 
the thigh. But the main use of the muscle is not so much 
to abduct the thigh, as to act from the thigh as a fixed point 
upon the pelvis. The muscle of one side acting inclines the 
pelvis to that side; the muscles of both sides acting, prevent 
inclination of the pelvis. When the glusetus medius of one 
side is paralyzed, the patient keeps his trunk bent toward 
that side in walking; when both sides are affected, he 
inclines alternately from one side to the other. The foot, 
too, is apt to turn outward, the gluteus medius being an 
internal rotator of the thigh. 

Movements at the Knee-joint. — The quadriceps femoris 
is the sole extensor. It is not used in standing (the 
patella can be felt to be loose then), but in walking it straight- 

* In the semi-flexed position of the thigh (as in sitting) this group of 
muscles act as abductors. 



THE LOWER LIMB. 1 87 

ens out the advanced leg just as this receives the weight of the 
body. When these muscles are paralyzed, the patient in 
walking has to avoid flexing his knees, lest he should be unable 
to straighten them again or unable to prevent further flexion 
of them by the body-weight, consequently he walks with 
straight knees, short steps, and with the body leaning forward. 
He cannot rise from the kneeling posture nor walk up stairs. 
Flexion of the knee is performed chiefly by the hamstrings ; 
of these, the biceps acts also as a powerful external rotator of 
the leg, the semi-tendinosus as a feeble internal rotator. To 
make up for this disparity, the anconeus, a feeble flexor, is a 
powerful internal rotator. The hamstrings acting from below 
extend the pelvis on the thigh, both in walking and in stand- 
ing. When they are paralyzed, the patient stands and walks 
with the trunk thrown back (trying to counterbalance by the 
body-weight the loss of extensor power at the hip). More- 
over, being unable to flex his knees sufficiently to clear his 
toes of the ground, he turns up his feet and toes excessively. 
The sartorius simultaneously flexes the hip and knee-joint. 
In walking this double flexion takes place in the backward leg 
just as it leaves the ground to be swung forward. The gracilis 
adducts the thigh, flexes the leg, and rotates it inward. 

Movements of Ankle and Toes. — Confusion is liable 
to arise from the fact that "extension" of the ankle-joint 
denotes a movement in just the opposite direction to " exten- 
sion " of the toes. To avoid this, it has been proposed to 
call the upward movement, whether of foot or toes, " dorsi- 
flexion," the opposite movement " plantar flexion." 

In plantar flexion of the foot the main agent is the muscu- 
lar mass which terminates in the tendo-Achillis — viz., the 
gastrocnemius and soleus. It acts chiefly on the back part of 
the foot, and has, besides, a tendency to adductand invert the 
foot. These muscles bear the greater part of the body-weight 
as the heel is raised, and paralysis of them will render walking 
impossible. The other agent is the peroneus longus. The 



I 88 NERVOUS DISEASES. 

plantar flexion produced by it is less powerful, but it draws 
downward strongly the inner and anterior part of the foot, 
planting this part firmly against the ground, while the gastroc- 
nemius is raising the heel. Its action on the unsupported 
foot is to (plantar) flex, abduct, and evert it ; and its tendon 
running obliquely across the sole braces up the plantar arch. 
Paralysis of this muscle gives rise to flat-foot, with pain in the 
sole from pressure on the nerves. The foot becomes inverted 
during walking, and thus corns arise on its outer side. 

Dorsiflexion of Foot. — The tibialis anticus dorsiflexes the 
foot powerfully ; at the same time it draws the inner border 
of the foot upward and inward (in exactly the opposite direc- 
tion to the peroneuslongus). It thus dorsiflexes, adducts, and 
inverts the foot. The extensor communis digitorum dorsiflexes 
(extends) the first joint of the toes and the foot ; it also abducts 
and everts the foot. The extensor proprius pollicis dorsiflexes 
the first joint of the great toe, and feebly dorsiflexes and 
adducts the foot. Paralysis of this group of muscles as a 
whole causes " foot-drop or ankle-drop " (so commonly seen 
in peripheral neuritis). In walking, in order to clear the toes 
from the ground, the patient has to resort to exaggerated 
flexion of the knee, which gives him a kind of high-stepping 
action. Paralysis of the tibialis anticus alone causes feebleness 
in dorsiflexing the foot, which is also abducted by the extensor 
communis digitorum. 

Simple abduction of the foot, without flexion in either 
direction, is produced by the peroneus brevis ; simple adduc- 
tion by the tibialis posticus. 

The manner in which toe movements are produced is analo- 
gous to that of finger movements. Thus, while the long 
extensor muscles extend (dorsiflex) the first phalanges and the 
long and short flexors flex the second and third phalanges, it 
is the office of the interossei and short muscles of the little 
and great toes to flex the first phalanges, keeping the second 
and third phalanges straight. This particular action of flexion 



THE LOWER LIMB. I «9 

at the first joints with extension of the other joints takes 
place whenever the weight of the body is maintained on the 
toes, and it enables the whole length of the toes, and not 
merely their last phalanges, to remain in contact with the 
ground. For the great toe this is of special importance, and 
consequently most of the muscles of the great toe-ball have 
this action. The transverse muscles of the foot act as a mus- 
cular ligament to the lateral arch of the metatarsals, which 
the body-weight tends to flatten out. Paralysis of the inter- 
ossei of the foot causes a distortion somewhat resembling the 
" main en griffe." 

Walking. — It is worth while to recapitulate in order the 
movements of the lower limbs in walking. Let us suppose 
that the right foot has been advanced and is about to receive 
the weight of the body from the left foot which is behind. 
The transfer necessitates a movement of the trunk forward 
and to the right. This is effected partly by the extension 
movement of the left leg (presently to be noticed), partly by 
the contraction of the right glutseus medius, which draws the 
pelvis over to the right : simultaneously the left erector spinas 
contracts, producing a slight compensatory movement of the 
vertebras, in order that the centre of gravity may not travel 
too fast or too far. As the right leg receives the body-weight, 
the right knee, at first slightly flexed, is forcibly straightened 
out by the quadriceps femoris. The hamstring muscles mod- 
erate this action, and also prevent the pelvis falling forward 
at the hip-joint. Meanwhile, in the hindmost (left) leg, the 
following processes have been going on : As the body comes 
forward the left hip becomes mechanically over-extended, the 
knee slightly flexed, and the foot somewhat dorsiflexed ; then 
comes a muscular movement of extension of the knee (quad- 
riceps, and especially rectus cruris), of plantar flexion of the 
foot (calf muscles, peroneus longus), and of the first phalan- 
geal joint of the toes (interossei, and short muscles of the 
toes). Thus, the joints of the left (hindmost) limb are 



I9O NERVOUS DISEASES. 

straightened out all along the line, and the necessary forward 
impulse is given to the body. The weight thus transferred to 
the right leg, the next action is to bring the left (hindmost) 
leg to the front ; for this the thigh is swung forward and then 
flexed on the pelvis (sartorius, ilio-psoas, tensor fasciae 
femoris) ; and in order that the toes may clear the ground, a 
series of movements in the opposite direction to those just 
described are made — viz., the knee-joint is flexed (sartorius, 
hamstrings) ; the foot and toes are dorsiflexed (tibialis anticus, 
extensor digitorum, extensor longus pollicis). After the 
foot has cleared the ground, the knee-joint is straightened 
again, till the foot is placed on the ground in front of the 
other. 

Distribution of Sensory Nerves in Lower Limb. — 
For the sensory nerve-supply of the lower limb we must refer 
to Fig. 57. It will be seen that — of the thigh — the external 
aspect is supplied by the external cutaneous ; the front aspect 
by the genito-crural above, the anterior crural (middle cuta- 
neous branch) below, and toward the inner side by the ante- 
rior crural (internal cutaneous branch), or by the obturator; 
the posterior aspect chiefly by the small sciatic ; the buttocks 
by the small sciatic below, by the lumbar and sacral nerves 
above ; the perineum by the pudic, associated with the inferior 
pudendal branch of the small sciatic on the scrotum or labia ; 
the front of the knee, by the patellar plexus from the anterior 
crural, external cutaneous, and obturator nerves. 

Of the leg — the inner aspect is supplied by the long saphe- 
nous branch of the anterior crural, the outer aspect by the 
peroneal (external popliteal) ; upon the front aspect these two 
nerve-districts meet in the middle line, but upon the posterior 
aspect they are separated near the back of the knee by the 
district of the small sciatic. 

The inner ankle is supplied by the long saphenous prolonged 
downward from the inner side of the leg ; the outer ankle 
(and outer side of foot and of little toe) by the short saphen- 



THE LOWER LIMB. 



I 9 I 



ous (a nerve which is made by the junction of branches from 
the internal and external popliteal nerves). 



Fig. 57 A. 



External cutaneous. 



Patellar plexus. 



External or short snphe 
nous. 




Ilio-inguinal. 

Ilio-hypogastnc. 
— Pudic. 

iddle cutaneous branch. 



Internal cutaneous branch 
of anterior crural. 



Internal or long saphe- 
nous from anterior crural. 



Musculo-cutaneous 

branch. 
Anterior tibial branch of 

peroneal. 



Diagram of the Cutaneous Nerve-Supply of the Lower Limb. 

{After Flower.) 

A. — Anterior Surface. 

In the foot the dorsum and dorsal aspect of the toes are 
supplied by the peroneal (external popliteal) nerve, the 



192 



NERVOUS DISEASES. 



adjacent sides of the great and second toes via its anterior 
tibial branch, the remainder via its musculo-cutaneous 



Lumbar and sacral. 



Pudic and small sciatic. 



Internal cutaneousbranch 
of anterior crural. 



Internal or long saphe- 
nous. 




Ilio-inguinal. 



External cutaneous. 



External or short saphe- 
nous. 



Posterior tibial. 



Diagram of the Cutaneous Nerve-Supply of the Lower Limb. 

{After Flower. ) 

B. — Posterior Surface. 



branch ; the sole and plantar aspect of toes are supplied by 
the internal popliteal nerve via its external and internal plantar 



THE LOWER LIMB. 



193 



branches, and then two branches divide this district after the 
fashion of the median and ulnar in the hand, the external 
plantar taking the outer part of the sole, the little toe, and 
adjacent side of fourth toe {cf. ulnar in hand), the internal 
plantar the remainder (cf. median). 

The Muscular Nerve-Supply is given in the following 
table : — 



TABLE OF MUSCULAR DISTRIBUTION OF NERVES IN LOWER LIMB. 



Separate twigs from 

lumbar nerves 
Obturator 



Anterior crural 



Separate twigs from 
sacral nerves 



Superior gluteal 

Inferior gluteal 
Sciatic nerve (main 

trunk) 
f Internal popliteal 
I division of sciatic 
I 
I via its posterior 



I via internal plan- 



via external plan- 
{ tar 

f External popliteal 

I division of sciatic 

or peroneal 

?-ia anterior tibial 
branch 



via musculo-cuta- 
rieous branch 



are distributed to Psoas 

" Muscles of adductor group, includ- 

ing pectineus and gracilis, ob- 
turator externus. 

" Uiacus, sartorius, pectineus. Qua- 

driceps extensor cruris. 



'.., pyriformis, 
femoris, ob- 



External rotators- 

gemelii, quadrai 

turator internus. 
Glutaeus medius and minimus. 

Tensor fasciae femoris. 
Glutaeus maximus. 

Hamstring muscles. Adductor 

magnus. 
Calf muscles — viz., gastrocnemius, 

soleus, plantaris. 

Tibialis posticus, flexor longus digi- 
torum, flexor longus hallucis, 
soleus. 

Abductor hallucis and flexor brevis 
hallucis, flexor brevis digitorum, 
and inner two lumbricales. 



The remaining plantar muscles. 



Tibialis anticus (per 
ticular branch). 

Tibialis anticus, extensor longus 
digitorum, extensor proprius pol- 
licis, peroneus tertius, and exten- 
sor brevis digitorum. 



" Peroneus longus, peroneus brevis. 

Disease limited to the individual nerve-trunks of the lower 
limb is less common than such disease in the upper limb, 
and wc shall not comment on each separately. 

Sciatica. — The common affection called sciatica calls for 



194 NERVOUS DISEASES. 

special notice. This is characterized by neuralgic pains 
extending along the course of the sciatic nerve and its 
branches. The pain may be dull and aching, or sharp and 
lancinating ; it is increased by pressure or tension on the 
nerve-trunk. This fact may be utilized for diagnosis as 
follows : Simple pressure upon the nerve where it leaves the 
pelvis between the tuber ischii and great trochanter evokes 
pain in a case of sciatica. But to be sure that such tender- 
ness is due to disease of the nerve and not of the hip- 
joint or neighboring parts, we may try the effect of tension 
thus. Put the patient on his back and flex the hip, 
first with the knee flexed, and secondly with the knee kept 
straight. The tension on the nerve, and consequently the 
pain, will be much greater when the hip is flexed with the 
knee straight. 

The movement of walking also stretches the nerve, and 
consequently the patient walks very carefully, trying to keep 
his hip-joint straight and his knee slightly flexed. Usually 
there is no paralysis, but cases do occur in which actual 
muscular weakness and even wasting supervene. Probably 
there is then not a mere neuralgia, but neuritis with destruction 
of nerve-fibres. 

The commonest causes of sciatica are exposure to cold, 
gout, rheumatism, nervous exhaustion due to overwork, to 
anxiety, to want of fresh air, and of proper food. The possi- 
bility of diabetes should be thought of. Syphilis has been 
alleged as a cause. Neither should we forget that sciatic pains 
(especially if accompanied by symptoms of true paralysis) may 
be symptomatic of new growth or inflammatory disease within 
the pelvis. Double sciatica, as a purely neuralgic affection, is 
rare, and should lead us to look, not only for intra-pelvic 
disease, but for disease of the lower part of the cord or its 
coverings. 

The treatment consists in- combating the constitutional 
cause where such can be found — thus, iodide of potassium, 



THE LOWER LIMB. IQ5 

alkalis, salicylate of soda, saline purges, etc., may be given in 
rheumatic or gouty cases ; quinine, iron, and other tonics, 
with change of air, in other cases ; and in local measures — rest 
to the limb; counter-irritants, such as blisters and mustard 
plasters ; anodynes, whether local, as morphia, cocaine, bella- 
donna, or by the mouth, as morphia, antipyrin, gelsemin. 
The constant current applied down the course of the nerve is 
sometimes very valuable. Yet many cases persist a long time 
refractory to all treatment. 



CHAPTER VI. 
NEURITIS. 

ORGANIC SPINAL DISEASES. 

The diagnosis of disease of a nerve-trunk must rest largely 
on anatomical considerations. We conclude that a given 
nerve is diseased because the area of paralysis, etc., corresponds 
with the known distribution of that nerve. But in practice 
this is not always so simply done, for the following reasons : 
(i) Disease of single nerve-trunks is less common than might 
be imagined ; for constitutional causes may affect more than 
one nerve at a time, or may affect the trunks higher up when 
they form the plexuses. (2) Sensory symptoms, notably 
anaesthesia, do not always give us the assistance which we 
might expect from them. For some unexplained reason, 
anaesthesia is often less marked and more fugitive than 
muscular paralysis. Neither does its grouping always corre- 
spond accurately with anatomical teaching; perhaps because 
the distribution of sensory nerves may vary in individual 
cases, or perhaps because the functions of a disabled nerve 
may be taken on by its neighbors. (3) Even muscular 
paralysis may not extend fully over the distribution of the 
nerve in cases where this is not completely severed. It 
behooves us, therefore, to consider, as well as its distribution, 
the other clinical phenomena of nerve-trunk disease. 

Acute Neuritis. — An acute neuritis, or inflammation of 
a nerve-trunk, affects primarily its sheath or interstitial tissue. 
These parts become congested, swollen, and infiltrated with 
cells. Hence pain at the seat of the disease (from the impli- 
cation of the nervi nervorum), and the presence, sometimes 
196 



ACUTE NEURITIS PERIPHERAL NEURITIS. I97 

ascertainable by touch, of an elongated, tender swelling of the 
nerve. As the nerve-fibres themselves become irritated, pains 
begin which are felt in the distribution of the nerve, are often 
very severe, and may have, like the pains of neuralgia, a 
periodic type. There may be extreme tenderness (hyper- 
gesthesia or hyperalgesia) not only of the nerve, but of the 
parts supplied by it. To these symptoms of irritation suc- 
ceed those of destruction of the nerve-fibres — viz., anaesthesia 
and paralysis in the district supplied by them ; then 
those of neuro-muscular degeneration — viz., wasting of 
muscle and reaction of degeneration. Pain, and particularly 
the burning pain known as " causalgia," may persist even in 
anaesthetic parts. Trophic changes may show themselves in 
other parts than the muscles, chiefly in the skin and nails. 
Thus, the nails become thickened, incurved, and talon-like ; 
the finger-ends tapering, and their skin thin, tense, smooth, and 
shining red (" glossy skin ") ; blebs may appear containing 
serous or sanious fluid which break and leave a deep ulcer. 
These latter symptoms probably denote a continued irritation 
of the nerve. Neuritis may be connected with the following 
causes : injury ; exposure to cold ; constitutional causes, such 
as rheumatism, gout, syphilis, diabetes, and perhaps alcoholism. 
Leprosy localizes itself in the nerve- trunks; new growths may 
also affect them. The treatment of neuritis will run on the 
same lines as that of neuralgia — viz., to attack the constitu- 
tional cause ; to secure perfect rest and protection from jars 
and blows to the affected limb, and to relieve pain during the 
acute stage ; to apply blisters and counter-irritants. Mercury 
is recommended internally, even for simple cases; and there 
can be little doubt that the proper application of the constant 
current both to the nerve and to the muscles is of great service. 
Peripheral Neuritis. — By "peripheral" neuritis we 
mean disease which affects the nerves near their termination. 
It may ascend so as to affect the trunks or even the roots, but 
its primary and principal seat is in the finer branches. Its 
17 



I98 NERVOUS DISEASES. 

nature may be inflammatory or degenerative, or both. It 
affects the hands, feet, or limbs, with limitation to any one 
nerve-district ; is almost always bilateral, and sometimes 
spreads over the whole body. Therefore it is also called 
" multiple " peripheral neuritis. 

Typical Form (Alcoholic). — Since this subject, when 
treated fully, is one of great complexity, we shall describe 
principally the commonest type of it. In this the disease is 
due to prolonged excess in alcohol, usually taken as spirits. 
The patient is often a woman of middle age or past, who has 
been drinking in secret. Probably before the outbreak of 
paralysis she will have had such premonitory symptoms as 
cramps in the legs, tingling, tenderness, and pains which she 
will call rheumatism. Loss of power in the legs is the com- 
plaint for which she generally is brought to the doctor. As 
a rule this has developed gradually, but sometimes very 
rapidly, so as to suggest an acute myelitis. It is often 
ascribed to a "chill," indeed there seems reason to think 
that this is the determining cause sometimes. On examina- 
tion we find a paralysis of the legs which has the following 
characters. The paralyzed muscles are flaccid,* and (if the 
disease be advanced) are wasted, and usually show changes in 
their electrical reactions. f The tendon reactions are absent. 
Further, the paralysis specially affects the anterior tibial group 
of muscles, so that the patient cannot dorsiflex the foot and 
toes, and there is a characteristic dropping of the foot. The 
bladder and rectum act normally as a rule. Sensory symptoms 
are usually best seen in the early stage. Besides the spontaneous 

* There may be spasm of some muscles, notably the hamstring muscles. 
But there is no general rigidity, as in descending sclerosis after transverse 
dorsal myelitis. 

f Alterations of polar formula, and sometimes complete RD, are to be 
found; but less generally than in disease of a nerve-trunk. There is 
nearly always loss of faradic contractility and diminished reaction to 
galvanism. 



PERIPHERAL NEURITIS. 1 99 

pains and cramps already mentioned, the skin may be hyper- 
aesthetic, so that the patient complains of the least touch. 
This may pass off and leave anaesthesia. But a still more con- 
stant feature is tenderness to deep pressure of the nerve-trunks 
and of the muscles, particularly the calf-muscles. The anaes- 
thesia when it exists is limited to the distribution of no one 
nerve, but envelops the foot and lower leg like a stocking. 
As to the upper limbs, even if no complaint is made about 
them, careful examination may show that they are affected in 
a minor degree. Or the paralysis may obviously involve them 
also; and in bad cases even the trunk, face, cardiac, and 
respiratory nerves. Bedsores are exceptional. The ocular 
movements, pupillary reactions, and fundus oculi are generally 
normal ; but squint may occur, and sometimes nystagmus. 
The pulse is often frequent, with a tendency to irregularity. 
The mental condition is remarkable. The memory fails, par- 
ticularly for recent events ; the patient will write letters and 
sign checks twice over. She may give a connected history of 
her illness, but on further inquiry it proves quite erroneous. 
She seldom appreciates her real condition, for she will describe 
how she went walking, shopping, etc., yesterday, when she 
was actually unable to move. She may not recognize the 
place where she is. Sometimes, however, there is marked 
hebetude, and in rarer cases delusions and delirium. 

The essential point in treatment is to enforce abstinence 
from alcohol. For this it will be advisable, as a rule, to re- 
move the patient from home, and place her in a hospital or 
similar institution. Rest in bed, wholesome food, warmth, 
and anodyne applications for the painful limbs, will be requi- 
site at first, with the treatment of such gastric or other com- 
plications as may be present; and later, tonics, iodide of 
potassium, galvanism, and massage. If the capital point of 
abstinence from alcohol can be secured, even severe and long- 
standing cases may in course of time recover. But neverthe- 
less there are dangers to life, which we shall rank as follows: 



200 NERVOUS DISEASES. 

(i) The whole nervous system may, from chronic poisoning, 
be so degenerate, that the patient dies, we hardly know why. 
(2) The neuritis spreads to vital nerves, pneumogastric or re- 
spiratory. (3) Causes outside the nervous system produce 
death, notably (a) phthisis, a possible accompaniment of 
peripheral neuritis, which should always be borne in mind ; 
(/?) dilatation of the heart ; (y) cirrhosis of the liver. 

As to the morbid anatomy of this disease : the changes in 
the central nervous system (such, that is, as might be held to 
stand in direct connection with the neuritis) are slight, if any ; 
the nerves to the naked eye may be normal, or may look 
swollen and reddened, or, in very chronic cases, gray and 
small. The microscope shows in them two sets of changes — 
(a) in the connective-tissue sheaths and endoneurium, infiltra- 
tion with cells or connective-tissue overgrowth — that is to say, 
the results of inflammation ; (/?) in the nerve-fibres, breaking 
up of the myeline into blocks and globules, with final absorp- 
tion of it, and disappearance (at any rate, in the advanced 
stages) of the axis cylinders — that is to say, degenerative 
changes. As yet we hardly know whether the inflammatory 
or the degenerative process be the primary, or whether they 
both go on side by side. We shall note two further points : 
(1) that infiltration with inflammatory cells has been seen in 
the muscles, as well as in the nerves. This may perhaps ex- 
plain the tenderness of the muscles. (2) That if the axis 
cylinders of a nerve be destroyed by the disease, the nerve 
and muscle fibres below that point will fall into a state of sec- 
ondary (Waller ian) degeneration {vide p. 77). 

Other Forms. — Peripheral neuritis assumes other forms, 
and may be due to other causes. Here we can only briefly 
allude to them. As to their morbid anatomy, it seems that 
in some forms this may be more strictly degenerative and 
limited to the parenchyma of the fibres than in that we have 
described. Further, sometimes the motor fibres are affected, 
to the exclusion of the sensory ; and this may make the 



PERIPHERAL NEURITIS. 201 

clinical diagnosis of neuritis very difficult. Two groups may 
be made, if we divide these forms according to symptoms : 
(i) Ataxic. There is little muscular weakness ; the prominent 
features are unsteadiness of gait, and awkwardness of the 
hands. The tendon reactions are absent, there may be little 
or no wasting of muscle or change in electrical reaction. The 
diagnosis has to be made from tabes dorsalis (progressive 
locomotor ataxy). Post-diphtheritic paralysis and diabetic 
neuritis not unfrequently take this form. (2) Paralytic. 
There is obvious paralysis, the muscles become flaccid, may 
waste and show reaction of degeneration. The onset may 
be acute, sometimes with high fever, the paralysis reaching its 
maximum within a few days, or the disease may be less rapid 
and more progressive. The diagnosis has to be made from 
a general myelitis, from the obscure disease known as acute 
ascending paralysis (Landry's disease), or from affection of 
the anterior cornual cells of the cord, acute or chronic, and 
from such a polio-myelitis in the absence of, or after the dis- 
appearance of, distinct sensory symptoms, the diagnosis may 
be well nigh impossible. 

And Other Modes of Causation. — Many and various 
causes are assigned for peripheral neuritis. Some of these, 
like alcohol, are toxic in nature — viz, arsenic, carbon-bisul- 
phide (used by India-rubber workers), salts of copper, silver, 
etc. Lead palsy would be reckoned by some authorities 
under peripheral neuritis. Other causes consist of constitu- 
tional diseases, either chronic, as diabetes, syphilis, tubercle, 
the disease known as beriberi ; or febrile diseases, as diph- 
theria, typhoid, mumps, measles, etc. The neuritis may arise 
during or more commonly after the fever. Thirdly, periph- 
eral neuritis may occur as part of a more general nervous 
degeneration, notably in tabes dorsalis. Fourthly, it may be 
connected with exposure to cold ; and, lastly, there may be 
idiopathic cases — i.e., those whose origin is as yet undis- 
covered. 



202 NERVOUS DISEASES. 

Diphtheritic Paralysis. — Of the paralyses which form 
the sequelae of acute disease, the principal is post-diphtheritic 
paralysis. It is probable that this is in most instances a 
degeneration of the peripheral nerves, though not always and 
entirely so, for in some cases disease of the spinal motor cells 
has been demonstrated. One of its commonest and earliest 
manifestations is paralysis of the soft palate, causing the voice 
to become nasal, and fluids, when swallowed, to regurgitate 
through the nose. The natural movement of the palate, 
seen on pronouncing "eh " with an in-drawn breath, is lost. 
Such palsy of the palate may occur so soon after the primary 
disease as to suggest that a local damage has been wrought 
by the inflammation. But that the damage is more than 
local is shown by the affection of other parts. Ocular 
paralyses are seen ; most commonly a paralysis of the accom- 
modation, so that the patient has difficulty in reading small 
type, less frequently palsy of the external ocular muscles, 
giving rise to squint ; or perhaps a paralysis of associated 
movements, so that the eyes cannot be converged, moved 
upward, etc. ; or perhaps there may be total ophthalmoplegia 
externa. Further, there is affection of the limbs. Although 
a well-defined anaesthesia is not present, there is often numb- 
ness, tingling, and perhaps blunting of sensation ; there may 
even be tenderness of the nerve trunks to pressure. And 
there is either (as we have said) a definite loss of power, or 
else an ataxic condition of the limbs. In either case the 
patellar tendon reaction disappears. Diphtheritic paralysis 
varies considerably in severity ; there may be little more than 
palsy of the palate, coupled with loss of knee jerk, or the 
patient may be quite unable to stand. The usual course is 
favorable ; the disease clears up gradually and disappears 
without sequela?. But sometimes, particularly in children, 
death may occur. This mostly results, it would seem, from 
implication of the respiratory and cardiac nerves or centres. 
Hence we must consider the following signs to be of serious 



DIPHTHERITIC PALSY LEAD PALSY. 2C>3 

import : paralysis of the diaphragm, vomiting, frequent, feeble, 
irregular pulse, dyspnoea without apparent cause, or morbid 
modifications of respiration. Iron, strychnine, massage, and 
electricity to the limbs are the means usually employed in 
treating diphtheritic paralysis. 

Lead Paralysis. — The morbid anatomy of lead paraly- 
sis is still somewhat uncertain. That there is some organic 
change, and that this lies either in the nerves or in the spinal 
motor cells, we should infer from the wasting and electrical 
changes in the muscles. The paralysis may in some instances, 
like alcoholic paralysis, manifest itself suddenly, but as a 
rule, the onset is- gradual. It has, in typical cases, a charac- 
teristic localization — viz., in the extensor muscles of the 
wrists and fingers, more particularly the extensor communis 
digitorum. If this muscle be paralyzed on both sides, with- 
out affection of sensation, and the adjacent supinator longus 
be at the same time sound, the probability of lead paralysis 
is very great, even apart from a corroborative blue line on the 
gums and a history of lead poisoning. For wrist-drop 
suggests lead even more surely than foot-drop suggests 
alcohol. The affected muscles waste, and show electrically 
reaction of degeneration, and that usually in a very typical 
fashion. There is no anaesthesia. The paralysis may spread 
further than this, to the hand-muscles, those of the upper 
arm, or it may, in severe cases, be more or less general. 
Sometimes it may be abnormal in distribution, affecting, for 
instance the upper arm, where it spares the forearm. There 
is, for the most part, little danger to life ; on the other hand, 
the paralysis is often very chronic and intractable, and after 
apparent cure, even at a long interval, it may break out again 
without obvious cause. Neither must it be forgotten that the 
lead may affect the nervous system in other ways, producing 
sometimes tremors, sometimes epileptic fits, sometimes a 
condition resembling general paralysis of the insane. We 
must remember, too, the predisposition of patients suffering 



204 NERVOUS DISEASES. 

from chronic lead poisoning to renal disease, and examine 
the urine, the heart, and the vascular system. For the treat- 
ment of paralysis itself galvanism is generally used, while 
iodide of potassium and a daily dose of sulphate of magnesia 
are given to remove the lead from the system. 

DISEASE OF THE ENVELOPS OF THE CORD. 

Acute Spinal Meningitis. — An acute general spinal 
meningitis is described as taking place either from exposure 
to cold (" rheumatic " ), or from unknown causes ("idio- 
pathic"). This is certainly uncommon; more usually it 
results from some specific disease, as, for instance, tubercle, 
syphilis, pyaemia, fevers, such as small-pox, typhus, etc., etc., 
or the disease known as epidemic cerebro-spinal meningitis. 
But in such cases a cerebral meningitis may co-exist and 
obscure the symptoms of the spinal disorder. Disease and 
injury of the neighboring parts, such as the vertebras, may 
also set up meningitis. 

An acute spinal meningitis affects the pia and arachnoid ; 
and in a well-marked example the surface of the cord (after 
opening the dural sheath) is found lined with inflammatory 
lymph, or even pus, held mostly in the meshes of the arach- 
noid. The inflammation may penetrate the surface of the 
cord, causing softening of its periphery (meningo-myelitis), 
and possibly of the deeper parts. The nerve-roots may be 
similarly affected. The symptoms are as follows : — 

Rigors, pyrexia, and other symptoms of severe internal in- 
flammation. 

Pain in the back, often very severe ; lancinating pains, 
tenderness, and paraesthesia in the limbs. Movement, and 
particularly the movement of rotating the vertebrae, makes 
the pain much worse. 

The muscles of the back are rigid, and when the upper parts 
of the cord are affected there is retraction of the head. 

There may be at first no actual paralysis, but movement is 



SPINAL MENINGITIS. 205 

difficult on account of the pain and stiffness. Later, if the 
nerve-roots or cord be damaged, paralysis, with muscular 
wasting and reaction of degeneration will supervene. 

For a like reason the tendon-reactions are generally an- 
nulled. 

There may be retention of urine and faeces. 

The patient may die during the height of the disease ; or 
he may, in a favorable case, entirely recover ; or he may die 
at a later stage from the effects of softening of the cord (bed- 
sores, cystitis, and the like) ; or he may recover with paralyzed 
and wasted limbs. In this last case, should the wasting be 
due to nerve-root lesion rather than to cord lesion, there is 
hope that it may eventually disappear. 

For treatment, in addition to general measures (such as are 
calculated to afford to the patient perfect rest, relief of pain, 
and assuagement of fever), mercury has been recommended, 
even in non-syphilitic cases; also iodide of potassium, spinal 
ice-bags, counter-irritants to the spine (applied with caution). 
After recovery, galvanism and massage will probably be of 
much use for the relief of paralysis. 

Tubercular spinal meningitis usually occurs as an adjunct 
and subsidiary to the cerebral disease ; but sometimes the 
conditions are reversed, the main symptom being a paraplegia 
which spreads upward and proves fatal. 

Syphilitic meningitis may be acute or subacute; it is more 
likely to be localized than the other forms. Nevertheless, in 
syphilitic subjects a meningitis occurs which spreads over the 
whole surface of the cord, and possibly of the brain also, with 
great rapidity. Mercurials and iodide must be pushed vigor- 
ously, and are here of undoubted value. 

Chronic Spinal Meningitis. — A chronic meningitis 
affecting the pia mater and arachnoid may be the result of 
chronic alcoholism. The membranes become thickened and 
matted, the cord is liable to be damaged, from injury to its 
vessels. The symptoms are spread over a longer period, and 
18 



206 NERVOUS DISEASES. 

the true cause of the pains, etc., may be only apparent after 
paralysis has begun to set in. 

Affections of Spinal Dura Mater. — As to diseases 
originating from the spinal dura mater, they are not common. 
Gummata may grow from its internal surface. A peculiar 
disease, consisting of (inflammatory ?) thickening, which 
spreads inward from the dura, and usually affects the cervical 
enlargement, causing a fusiform swelling in this region, is 
called by Charcot "cervical pachymeningitis." It develops 
gradually, causing at first pains and paresthesia in the hands 
and arms, then, as the nerve-roots begin to perish, paralysis with 
wasting and anaesthesia. The paralysis usually has this pecu- 
liarity, that it affects the district of the ulnar and median 
nerves, but not the musculo-spiral, so that the hand and first 
joints of the fingers are hyper-extended while the small hand 
muscles are wasted. As the cord becomes pressed upon, para- 
plegia develops. This spinal pachymeningitis is certainly 
uncommon. 

Effects of Vertebral Caries (Pott's Disease.) — 
Much more important, because much more common, is the 
paralysis which may accompany caries of the vertebrae. 
Caries of the vertebrae may be accompanied by two sets of 
symptoms: (i) those which appeal chiefly to the surgeon — 
viz., pain and tenderness to handling of the affected vertebrae, 
and, in addition, the well-known angular curvature ; (2) 
symptoms indicating disease of the cord and possibly nerve- 
roots, at the level of the vertebral disease. It is natural, 
at first sight, to suppose that these latter symptoms are due to 
mechanical distortion of the cord from curvature. This is not 
so, or not wholly so, for paralysis may be present with very 
slight curvature, and absent when the curvature is great. The 
paralysis is generally due to a " compression myelitis" (vide 
p. 86), i. e., upon the diseased bones, within the spinal canal, 
inflammatory and caseating material is heaped up, which 
gradually compresses and invades the membranes and the cord. 



CARIES OF VERTEBR/E. 2C>7 

The nerve symptoms consist in paraplegia, gradual in onset, 
of the parts below, affecting first and principally the motor 
functions, and next the sensory. The bladder and rectum 
are paralyzed in bad cases. There may or may not be at the 
onset symptoms indicative of interference with the nerve-roots 
at the level of the caries — viz., pain and hyperaesthesia with 
paralysis in their distribution. Usually such " root-symptoms " 
are not marked, unless the disease happens to affect the nerve- 
roots of the brachial plexus, but more commonly the caries is 
in the dorsal region. Thus the nervous symptoms indicate 
only transverse disease of the cord at a particular level, usually 
the dorsal region ; they do not tell us the nature of the dis- 
ease. This is inferred from the vertebral symptoms, princi- 
pally from the curvature. Hence the importance of examin- 
ing the spinal column in all cases of paraplegia. 

Some remarks may be made, however, on the characters of 
the paraplegia, (i) It is, like all paraplegia from disease of 
the dorsal cord, " spastic " in type. The legs are dragged if 
the patient can still walk, and they become rigid. The reflex 
actions are exaggerated, and perhaps more so in this paralysis 
from compression than in any form of spastic paraplegia. 
Very excessive knee-jerk, very marked ankle-clonus, and 
excessive plantar reflex are seen even with moderate paralysis. 
(2) The degree of sensory paralysis may serve more or less 
as an index of the damage to the cord. Complete anaesthesia 
indicates grave mischief, and with it usually come the serious 
complications of cystitis, bedsores, etc. Even bad cases, 
however, are more hopeful than paraplegiae from disease 
originating in the cord ; for the mischief may arise from com- 
pression rather than destruction, and then recovery is still 
possible. It need hardly be added that the symptoms will 
vary according to the part of the cord which is affected (vide 
p. 210, transverse myelitis. Should the upper cervical verte- 
brae be carious, there is the danger of sudden death from dis- 
location caused by the weight of the head. The treatment 



208 NERVOUS DISEASES. 

indicated for paralysis associated with vertebral caries is abso- 
lute and prolonged rest in bed, to allow the caries to subside 
and the vertebrae to consolidate themselves, for usually in this 
case the secondary affection will subside also ; cod-liver oil, 
tonics, and feeding suitable for strumous patients ; then surgi- 
cal measures, such as spinal jackets and supports, for the relief 
of the bone disease. By some, the application of the actual 
cautery to the skin of the back is recommended while the 
disease is still in progress. In old-standing, obstinate cases 
it may be considered whether opening the spinal column, 
with the design of removing material which may be pressing 
on the cord, will offer prospect of relief. 

Effects of Vertebral Cancer. — We shall here only 
mention a second form of vertebral disease, luckily less com- 
mon than the preceding. This is cancer of the vertebrae. 
Like caries, it causes paralysis of the parts below by invasion 
of the cord ; but it is distinguished by the extreme severity 
of the pain which accompanies its progress. This has earned 
for the disease the name of " paraplegia dolorosa." 

DISEASES OF THE SPINAL CORD. 

Classification. — Diseases of the spinal cord itself may be 
classified in various ways. They may depend upon an acute 
softening (inflammatory or necrotic), or upon a more chronic 
inflammation. This group falls under the head of " myelitis." 
They may, on the other hand, depend on a degenerative pro- 
cess ; this may be secondary or primary, as we have already 
said {vide pp. 78, 82). But between chronic inflammation 
and degeneration it is difficult to draw a line. 

Again, spinal disease may be selective, discriminative, or 
" systematic " — /. e., limiting itself to those tracts or areas of 
the cord which (we have reason to think) constitute definite 
physiological or embryological systems. On the other hand, 
it may be non-selective, indiscriminate, or "diffuse," attack- 
ing the tissues and spreading in them without regard for such 



ACUTE GENERAL MYELITIS. 2O9 

boundaries. Most " system " diseases are degenerative, and 
most diffuse diseases inflammatory ; but there may be excep- 
tions. Lastly (turning to their mode of onset and cause), 
they may be, like all other diseases, acute, subacute, or chronic. 
(We omit for the present the subjects of syphilis and new- 
growths affecting the cord.) 

It is useful to bear these distinctions in mind, but con- 
venience of description, as well as the limited state of our 
knowledge concerning some diseases, forbids us to follow out 
such a classification too strictly. 

Under the term acute myelitis we shall here rank acute 
softening of the cord, whether from inflammation or from the 
necrosis which follows vascular obstruction. The processes 
are doubtless different, but it may be impossible to say which 
has been at work in a given case. For the net result in either 
case is softening, and the minute examination of softened 
nerve-tissue is somewhat unsatisfactory. An acute myelitis 
may be general — i.e., affecting a long length of cord; or 
local, affecting a short length only. Or there may be numer- 
ous small patches of myelitis scattered through the cord. This 
is called "disseminated myelitis." 

Acute General Myelitis is not common ; and fortu- 
nately so, for it is fraught with great danger to life. Exposure 
to cold, especially under circumstances of privation or over- 
work, is alleged to be the common cause. Other causes are 
— the infection of acute specific diseases, of pyemia, and per- 
haps syphilis. It may also be secondary to injury, or disease 
of the neighboring bones or membranes. Pain in the back 
and paralysis are the chief symptoms. The pain is much less 
severe than in meningitis. But the paralysis is an earlier and 
much more pronounced symptom than in meningitis. The 
muscles are flaccid, they soon show electrical reaction of de- 
generation, and begin to waste. The tendon-reactions are 
abolished. The bladder and rectum are paralyzed. There 
is paralysis of sensation ; absence of skin reflexes. Bedsores 



2IO NERVOUS DISEASES. 

and cystitis are apt to appear. Delirium and coma may super- 
vene, even apart from cerebral disease. In some exceptional 
cases optic neuritis has been seen. In the acute stage little 
more can be done than by careful nursing and feeding to keep 
the patient alive ; a water-bed should be used ; particular 
attention must be given to the skin of the back and the state 
of the bladder. Should the patient recover, the paralysis 
that is left must be treated like the similar sequelae of menin- 
gitis ; but the prospect of cure is not so good, since there has 
been destruction of nerve-centres, and not of nerve-roots only. 

Acute Ascending Paralysis (Landry's Disease). — 
We may here mention the disease known as acute ascending 
paralysis, or " Landry's disease." The symptoms suggest an 
acute, rapidly spreading myelitis, but no constant lesion has 
been found in the cord. Some say that the lesion is a multiple 
neuritis. The spleen is found to be enlarged ; hence it has 
been argued to be due to some acute specific disease ; nay, it 
is even said that micro-organisms have been detected in the 
peripheral nerves. Dr. Bristowe mentions a case which he 
thinks was a manifestation of hydrophobia. It manifests 
itself as a paralysis, beginning in the lower limbs and spread- 
ing rapidly upward. The precise order of its spread is said 
to be — muscles of toes and feet, posterior muscles of thigh 
and pelvis, anterior muscles of thigh ; muscles of fingers, 
scapular muscles, upper arm muscles ; trunk ; respiratory 
muscles ; muscles innervated from the medulla. The limbs are 
flaccid and the tendon-reactions absent ; but the electrical re- 
actions are normal. Again, though there be numbness and 
paresthesia;, there is no definite sensory paralysis. These 
features are said to distinguish it from acute general myelitis. 
It may terminate fatally in a few days, or within a week or 
two; some few cases recover. Large and frequent doses of 
ergotin are credited with having saved life in one case. 

Localized or Transverse Myelitis. — Local myelitis 
(7. (?., that which involves only a small length of cord), when 



TRANSVERSE MYELITIS. 2 I I 

it is acute will probably affect the whole thickness of the 
organ; for this reason it is called "transverse myelitis." 
(We must except, however, the acute affection of the anterior 
cornua, which we shall describe presently.) There is little to 
add concerning its causation, save that any deficiency of 
arterial blood-supply is likely to cause a local softening. 
Syphilis, a tolerably definite cause, may probably act in this 
way. The symptoms vary according to the level of the 
lesion, and according to its completeness. 

Of Dorsal Region. — By far the commonest level is the 
dorsal region. A complete, or as it is sometimes called a 
" total," transverse dorsal myelitis produces motor paralysis 
of the lower limbs, paralysis of the bladder and rectum, and 
sensory palsy of all parts up to the level of the lesion ; at the 
upper level of the anaesthesia there may be a zone of hyper- 
esthesia, or perhaps a "girdle pain." Acute bedsores are 
liable soon to form upon the sacrum. The condition of the 
lower limbs at first is this : they are flaccid, and the skin 
reflexes and tendon-reactions are abolished. According to 
most accounts this is due to "shock," but as time goes on, 
and more particularly as secondary lateral sclerosis develops, 
the tendon-reactions return and become exaggerated, and 
rigidity sets in. This is certainly true for cases where the 
severance of the cord has not been quite complete. Where 
it has been complete, it would appear that though the skin 
reflexes may return, the tendon-reactions remain absent, and 
the legs do not become rigid. But their electrical reactions 
are not (as in lumbar myelitis) abnormal. A complete trans- 
verse lesion will probably never recover ; in the milder cases 
sensation may return, the bladder may recover itself, often 
imperfectly, and motor power be more or less regained in the 
legs. The patient walks with his legs held stiffly, dragging 
his feet after him instead of lifting them from the ground ; it 
is the gait of "spastic paraplegia." 



212 NERVOUS DISEASES. 

Of Lumbar or Cervical Enlargements. — Myelitis of 
the lumbar and cervical enlargements is characterized by the 
symptoms proper to destruction of the nerve-cells of these 
parts. Suppose the lumbo-sacral region of the cord destroyed, 
then not only are the legs, bladder, rectum, and nervi erigentes 
paralyzed, but the muscles, instead of becoming rigid, are at 
first flaccid ; then show degenerative changes to electrical 
tests ; then waste ; the skin reflexes and tendon-reactions are 
alike permanently abolished. The anaesthesia will correspond 
to the distribution of the lumbar and sacral nerve-roots (vide 
p. 23). Similarly an affection of the cervical enlargement 
will cause a wasting paralysis of the arms, with a spastic para- 
plegia of the legs. 

Chronic Myelitis. — In chronic myelitis the morbid pro- 
cess falls principally on the connective tissue and neuroglia. 
By the overgrowth of these tissues the nerve elements are, so 
to speak, choked. The general result is not softening, but 
induration ; and except by the distribution of the lesions, it 
may be difficult to tell whether we have to do with a chronic 
inflammation or a chronic degeneration. Chronic alcoholism, 
vascular disease — whether from atheroma, from renal disease, 
or other source — and syphilis rank among the causes. The 
symptoms will be regulated, as in acute myelitis, principally 
by the position of the lesion. They will differ from those of 
acute myelitis chiefly in their gradual onset, and in the fact 
that they are more apt to be heralded by symptoms of irrita- 
tion, such as pains, paresthesias, cramps, and twitchings. In 
the early stages it may be difficult to say with what complaint 
we have to deal. 

Acute Anterior Cornual Myelitis or Infantile Spinal 
Paralysis. — Acute disease of the anterior gray cornua is known 
as acute anterior polio-myelitis, or anterior cornual myelitis, or 
acute atrophic paralysis, or sometimes simply as infantile paraly- 
sis (spinal form). It differs from the forms of myelitis we have 



ANTERIOR POLIO-MYELITIS. 21 3 

just considered in that it is selective, limiting itself to the 
anterior horns of the gray matter. But probably this limita- 
tion is due to the fact that these parts have a particularly free 
blood-supply; for there is reason to think (from the few 
examinations that have been made at an early stage of the 
disease) that the process is one of acute inflammation. It is 
common in early childhood ; it occurs, but with far less fre- 
quency, in adults. Its causes are practically unknown. 
Generally the child is taken suddenly ill, with more or less 
fever, vomiting, and perhaps convulsions. It is put to bed, 
and perhaps no diagnosis can be made at first. In a day or 
two probably the paralysis will be noticed. The extent of it 
varies in different cases. One or more limbs may be involved, 
or even the trunk muscles, so that the child cannot sit up or 
hold its head up. The face and tongue are scarcely ever 
affected. But the maximum is reached either at once or 
within a very short time. Then begins what may be called 
the "regressive stage." Motor power gradually returns in 
one part after another till the paralysis is narrowed down, it 
may be, to one or more limbs, or even to a part of one limb. 
The distribution quoad the limbs may vary. One leg, one 
arm, both legs, arm and leg of same side, may be affected. 
Within the limbs certain groups of muscles may be picked 
out in a manner that is suggestive of spinal cord disease ; for 
instance, in the upper limb the muscles of hand and forearm, 
or the deltoid spinati and flexors of elbow-joint ; in the lower 
limb, the anterior tibial group, or the calf muscles, or the 
thigh muscles. Within a fortnight, or earlier, the electro- 
contractility begins to alter,* and next the muscles waste. 
This wasting marks out to the eye the localized character of 
the disease. The bladder and rectum usually escape. The 

*This is a point useful in prognosis. If after a fortnight a muscle 
retains its farado-contractility, its spinal centre is not destroyed, and we 
may count on its recovery. 



214 NERVOUS DISEASES. 

tendon-reactions and the skin reflexes (so far as they require 
the co-operation of the paralyzed muscles) are abolished. 
But sensation remains perfectly normal. 

There comes a time when the "regression" of the par- 
alysis ceases. Even in mild cases it is probable that some 
permanent disability will be left. In severer cases, as time 
goes on, not only do the muscles waste, but the bones of the 
affected limb are checked in their development, so that it 
becomes shorter than its fellow. Vaso-motor paralysis is seen, 
the skin becomes cold, purplish, and subject to chilblains. 
Deformities of the foot arise, mainly from the unbalanced 
action of non-paralyzed muscles; this disease is a fruitful 
source of club-foot. 

As to treatment, the damage to the cord will have occurred, 
most likely, before the diagnostic symptom of paralysis has 
shown itself. We cannot repair the destruction of cells; but 
we try to facilitate recovery by maintaining the nutrition of 
the paralyzed parts. The limb must be kept warm from the 
first, and after three or four weeks massage and electricity 
should be regularly applied. The constant current should be 
used ; both because it dilates the blood-vessels of the part, 
and because the muscles will contract under it and not under 
faradism. Even at a late stage such measures will do some 
good. The child should be encouraged to use the limb ; and 
if deformities have arisen, tenotomies may be practiced, and 
surgical boots applied, to enable him to use it the better. 

The same disease occurs, though exceptionally, in adults. 

Subacute Form. — A subacute form of anterior polio- 
myelitis is known. It differs from the acute form in the 
more gradual character of its onset. It is more common in 
adults than in children. It has to be distinguished from a 
multiple neuritis. 

Tabes Dorsalis — Locomotor Ataxy — Posterior 
Sclerosis. — Tabes dorsalis or locomotor ataxy consists, to 
speak roughly, of a chronic degeneration or "sclerosis" of 



LOCOMOTOR ATAXY. 21$ 

the posterior columns of the cord. These parts are affected 
as follows : The postero-lateral column degenerates first at 
the point where the entering posterior nerve-roots course 
through it (posterior root-zone), in the lumbo-dorsal region 
to begin with, and then at higher levels. This degeneration 
is primary, so far as we know. Next there occurs a secondary 

Fig. 58. 

i :-•-, ,-"-, c~jiT~ 'Cervical enlargement. 



. CeTvical enlargemen 




Upper dorsal region. 



Lower dorsal region. 



Tabes Dorsalis. 
In the two lowest sections the whole posterior columns are diseased ; in the centre sec- 
tion nearly the whole of them ; in the two upper sections the disease lies chiefly or 
solely in the postero-median columns. 

degeneration in the postero-median column, starting from 
the level of the primary degeneration (wherein it originates), 
and reaching up through the whole length of the cord. Thus, 
in the lower dorsal region the whole sectional area of the pos- 
terior columns may be involved ; in the cervical region only 
the postero-median part of it (columns of Goll). In rare in- 
stances the primary degeneration begins in the cervical region 



2l6 NERVOUS DISEASES. 

of the cord, and not in the lower dorsal region. The pos- 
terior nerve-roots are often diseased as well ; indeed, it may 
be argued that the primary disease begins here. Other parts 
of the cord may be affected : Lissauer's columns frequently, 
and at an early stage, it is said ; the vesicular columns of 
Clarke, and (probably in connection with them) the direct 
cerebellar tract ; also the antero-lateral ascending tract. All 
these parts, it will be noted, consist of centripetal fibres. 
The degeneration may spread from the posterior columns to 
the posterior horns of gray matter. In some rare cases the 
anterior cornual cells also degenerate. Lastly, recent re- 
searches show that a degeneration of peripheral nerve-fibres 
is by no means uncommon in tabes. 

There are few diseases in which such a variety of seemingly 
disconnected symptoms may arise. We will first describe an 
orthodox type of case, and then give an account of the ac- 
cessory (though often more prominent) symptoms. 

Typical Form. — The patient is usually a man of middle 
age, or past it ; and he will complain of difficulty in walking. 
His gait is unsteady, especially as he turns; he looks at his 
feet as he walks, to prevent falling. In advanced cases (chiefly 
where sensation is much impaired) there is a peculiar flourish- 
ing of the feet ; they are lifted higher than necessary, thrown 
forward and outward, and brought down on the heel with a 
stamp. (The patient has been said to "walk like a cock.") 
When made to stand with his feet together, he is unsteady ; 
and when in addition he shuts his eyes, he will fall (Rom- 
berg's symptom). These symptoms are due not so much 
to loss of power, as to want of harmony in the muscular 
actions necessary for walking, and hence the name "locomo- 
tor ataxia." Nevertheless, in many cases there is actual loss 
of power, and in some this becomes a prominent symptom. 
The inco-ordination may affect the hands, and then there 
is an awkwardness in fine movements, such as picking up 
a pin, fastening buttons, etc., and he cannot guide his fingers 



LOCOMOTOR ATAXY. 2\J 

without looking at them. If told to touch his nose with his 
finger quickly, he may do so ; but if he repeats the attempt 
with his eyes shut, he goes astray. The patient has, or has 
had at a previous date, severe pains. These may be of an 
aching, boring kind, or (what is more characteristic) of the 
kind known as " lightning pains " — sharp lancinating pains, 
of momentary duration, so far as each pain is concerned, but 
occurring in bouts that may last for a day or several days. 
Their usual seat is the legs, but they may appear in very various 
parts. They are not, like the pains of neuralgia or neuritis, 
limited to the course of any one nerve. They are ascribed to 
irritation of the posterior nerve-roots as they pass into the 
cord. In addition, there is anaesthesia, or more commonly a 
blunting of sensation in the legs, in consequence of which 
the patient feels as if he were walking on wool or on a thick 
carpet. One or all of the modes of sensation (enumerated 
on p. 99) may be affected. It is common to find loss of 
muscular sense ; the patient does not know how his legs are 
placed unless he looks at them. It is also common to find 
delay in the transmission of painful sensations. Often there 
is a girdle-pain. Examination will show the presence of two 
very important symptoms not known to the patient himself: 

(1) That the patellar tendon-reaction is completely absent, 
although the nutrition of the quadriceps cruris, and its elec- 
tro-contractility is normal (Westphal's sign). 

(2) That the pupils, which probably are small in size, fail 
to contract under the stimulus of light, though they contract 
well during convergence and accommodation (reflex irido- 
plegia, or Argyll-Robertson's sign). 

Stages. — Such is the condition presented by a somewhat 
advanced stage of the disease. Patients often come to us at 
earlier stages, either when the gait is merely unsteady, or 
even when there is no apparent difficulty of walking. This 
latter has been called the " pre-ataxic stage." The symptoms 
which then attract the patient's attention are, first, the pains; 



2l8 NERVOUS DISEASES. 

secondly, some of the accessory symptoms, of which we shall 
presently speak. The commonest of these are — transitory 
paralysis of the ocular muscles, giving rise to squint or 
ptosis, or difficulties of micturition, usually consisting of a 
lack of complete control over the sphincter of the bladder. 
For diagnosis we must look for three main symptoms : (i) 
the characteristic pains, (2) the absence of patellar-tendon 
reflex, (3) the " Argyll-Robertson pupils." Where all three 
are present, the diagnosis of tabes may be made ; when 
one or other fails (it is usually the pupil-sign), we can only 
surmise, and confirm our surmise by the presence of acces- 
sory symptoms. 

The disease is progressive as a rule — from the pre-ataxic stage 
it passes to that of complete ataxia, and then to the paralytic 
stage. In this last stage the patient becomes unable to stand 
or walk, and the advent of cystitis or of bedsores may end 
his days. Nevertheless, the progress of the disease is, in most 
cases, very slow, being measured by years, and it may stop 
short at any stage. Even when it does not so stop, some 
early symptoms, such as the pains, often pass off as the ataxia 
develops. 

Accessory and Anomalous Symptoms. — We must 
now turn to the accessory symptoms. These are very various, 
and often so obtrusive as to mask the real character of the 
disease. As to the organs of special sense, we have already 
mentioned the condition of the pupil and ocular paralysis. 
Sometimes there is complete ophthalmoplegia. Optic atrophy 
is a tolerably common event, and may be one of the first 
symptoms. It produces limitations of the field of vision, 
color-blindness, amaurosis, and finally complete blindness. 
Many patients with tabes will be found, on examination, to 
hear imperfectly. The reason may be doubtful, for they 
often have an opaque and thickened membrana tympani, 
indicating a chronic dry catarrh of the tympanum ; but in 
some cases, at any rate, the perosseous hearing is imperfect, 



LOCOMOTOR ATAXY. 2IO. 

and the mischief presumably nervous. Vertigo, another symp- 
tom of this disease, may be due either to the aural condition 
or to ocular paralysis, or to the loss of muscular sense. 

The pains, as we have said, may occur in other places than 
the legs. With the pains, and resembling them in their 
paroxysmal character, are associated disturbances of various 
internal organs, known as "crises." A gastric crisis may 
begin with lightning pains between the scapulse, which work 
their way round to the epigastrium ; then vomiting sets in, and 
for several days, it may be, the patient vomits after taking 
food or drink, or even without this. A "rectal crisis " con- 
sists of tenesmus and pain at the lower bowel, followed, it 
may be, by diarrhoea, or even bloody stools. Similarly ure- 
thral, bronchial, and pharyngeal crises have been described. 
As to the vascular system, an undue frequency of pulse has 
been noted ; further, there is often valvular (usually aortic) 
disease. Ecchymoses, sometimes large, sometimes in the 
form of purpuric spots, have been seen, particularly after a 
bout of pains. Difficulties of micturition we have noticed as 
a common early symptom ; in the. genital system there has 
been observed, in the early stages, increase of sexual desire 
with a capacity for frequent satisfaction not evinced in healthy 
men ; .later, sexual impotence. 

The paralytic symptoms constitute an interesting group. 
Many of these occur early and are transitory ; ptosis and 
ocular paralysis are the commonest ; hemiplegia and para- 
plegia are also seen ; their anatomical basis we do not know. 
An important form of paralysis is bilateral paralysis of the 
abductors of the larynx {vide p. 165); this also may occur 
quite early in the disease. Paralysis with muscular wasting is 
seen sometimes ; as, for instance, in one-half of the tongue, or 
in the limbs. This may either be due to a neuritis, or to 
spread of the central degeneration into the motor cells of the 
cord or medulla. Under trophic lesions we may reckon : 

(1) Perforating ulcer of the foot; this is generally asso- 



220 NERVOUS DISEASES. 

ciated with anaesthesia, or at least some sensory disturbance 
of the part ; it may recover, sometimes quite rapidly. 

(2) Disease of bones and joints ; the bones become fragile 
and liable to fracture from very slight causes, or a joint be- 
comes suddenly swollen, the swelling extending, it may be, 
into the adjacent tissues of the limb. The swelling may subside 
without much further damage, or the disease may go on to com- 
plete destruction of the joint, leaving the limb " like a flail." 

(3) The nails and teeth may come out. 

Lastly, we must add that though mental symptoms form 
ordinarily no part of tabes, sometimes a state of mental exal- 
tation arises, and the patient may pass into a condition 
resembling general paralysis of the insane. This is one way 
in which tabes may terminate. 

As to the causation of tabes, syphilis is so frequent an ante- 
cedent, that it is commonly thought to be at least a predis- 
posing cause, although we do not understand its mode of 
action. Exposure to cold, and injury to the back or to other 
parts, have also been alleged as causes. The disease is much 
commoner in men than in women. 

Treatment is unsatisfactory, as is the case with most degen- 
erative nervous diseases. As to drugs, mercury and iodide of 
potassium have been used, but without the good results that 
would be wrought on a syphilitic inflammation or a gumma. 
Nevertheless, iodide of potassium is certainly useful. Nitrate 
of silver is recommended, and arsenic. For relief of the 
lightning pains antifebrin and antipyrin are very prompt and 
efficient remedies. A strong constant current applied from 
the spine to the feet appears to do good to some cases. 
Faradization of the spine with the wire-brush has been 
employed abroad. Suspension treatment appears to have had 
its day. In spite of apparent inefficacy of treatment, the fact 
that pauses and even arrests of the disease may occur naturally 
should lead us to persevere, in the hope that we may find a 
means of producing arrest artificially. 



SPASTIC PARAPLEGIA. 221 

Lateral Sclerosis, or Spastic Paraplegia. — Just as 
ataxia, with abolition of tendon reflexes, points to disease of 
the posterior columns of the cord (or, more strictly, to disease 
of the external part of these columns), so there are symptoms 
which point to disease of the lateral columns, or, strictly 
speaking, to that part of them known as the pyramidal tracts. 
These symptoms, as we have already mentioned, are loss of 
power in the limbs, with increase of tendon reflexes, and 
eventually rigidity. This condition is known, with reference 
to the lower limbs, as "spastic paraplegia." There is 
increasing weakness of the legs; in walking they are lifted 
insufficiently, so that the toes do not clear the ground, and 
the toes of the boots wear out ; as he gets worse, the patient 
has to walk very slowly, standing on the one leg with his body 
leaning forward, and dragging the other laboriously forward ; 
finally, the increasing weakness and rigidity prevent his 
walking at all, and his lower limbs become fixed, probably in 
the position of extension, with internal rotation of the thigh, 
though they may assume the (still more inconvenient) position 
of flexion at the hip and knee. Increase of tendon-reaction 
and ankle-clonus are marked, till the access of extreme 
rigidity prevents the production of them. The gradual onset 
of spastic paraplegia, followed by the development of similar 
phenomena in the arms, if unaccompanied by other spinal 
symptoms, is said, by eminent authorities, to be characteristic 
of a primary degeneration of the lateral columns (pyramidal 
tracts), just as locomotor ataxy is characteristic of primary 
degeneration of the posterior columns. And to such disease 
have been given the various names, "idiopathic lateral scle- 
rosis," " spasmodic tabes," or simply " spastic paraplegia." 
There are reasons, however, why we should be cautious in 
diagnosing pure "lateral sclerosis" during life. First, 
because the mere symptom of spastic paraplegia may occur in 
the course of, or even as the main manifestation of, several 
other diseases, such as transverse myelitis, or compression 



222 NERVOUS DISEASES. 

myelitis, of the dorsal cord; disseminated sclerosis; amyo- 
trophic lateral sclerosis (vide infra) ; hysteria. We must 
therefore exclude all symptoms referable to other parts than 
the pyramidal tracts, mainly, that is, sensory symptoms, affec- 
tions of the sphincters, trophic symptoms — viz., bedsores, 
muscular atrophy with reaction of degeneration, tremors, 
cerebral symptoms ; and must be certain (which is no easy 
matter) that we have to do with an unalloyed, slowly progres- 
sive, spastic paralysis of the limbs. Secondly, we must 
remember that although spastic paralysis of one kind or 
another is extremely common during life, an idiopathic lateral 
sclerosis is extremely rare post-mortem, so much so that its 
existence (except as an accessory to a more general nervous 
degeneration, such as general paralysis, or in combined 
degenerations of various spinal tracts) has been actually denied. 
Postero-Lateral (Combined) Sclerosis, or Ataxic 
Paraplegia. — It is possible for disease to develop in the 
posterior and in the lateral columns simultaneously. Such 
cases have been called (from the pathological point of view) 
" postero-lateral sclerosis," or "combined system disease; " 
or again, from the clinical point of view, " ataxic paraplegia." 
We may roughly distinguish two types : the first, in which the 
posterior columns are completely sclerosed, the disease involv- 
ing both external and median parts of the column ; while in 
the lateral columns there is sclerosis (but less intense and 
complete) of the pyramidal tracts. It is probable that such 
cases clinically will resemble true tabes, in that there is inco- 
ordination, with or without sensory symptoms, and absence of 
tendon-reactions. But to the inco-ordination is added loss of 
power, and the legs are dragged in walking, not tossed about. 
In the second type, the lateral sclerosis (degeneration of pyra- 
midal tracts) preponderates, while the posterior sclerosis is 
incomplete. Then the symptoms are mainly those of spastic 
paraplegia with exaggeration of tendon-reactions, while inco- 
ordination, sensory symptoms, bladder troubles, etc., may be 



ATAXIC PARAPLEGIA. 



223 



present in just such degree as to indicate the mixed nature of 
the affection. 

The clinical characters of a postero-lateral sclerosis consist 
therefore in a combination of the symptoms producible by- 
disease of the parts of the cord affected ; excepting perhaps in 
the behavior of the tendon-reactions. This (to speak only 



Fig. 59- 




Cervical enlargement. 



Cervical enlargement. 



Upper dorsal region. 



Upper lumbar region. 



Posterolateral Sclerosis. 

The posterior columns are completely degenerated, excepting in (1) a narrow zone 
abutting on the gray matter; (2) a small triangular area close to the apex of the 
posterior cornu, in the upper lumbar region. (This latter corresponds with the zone 
of entry of the posterior nerve-roots, and since it was healthy the knee-jerks were in 
this case retained.) 

The lateral columns show degeneration affecting in an irregular fashion(i) the cere- 
bellar tracts, chiefly in the cervical region. (2) The crossed pyramidal tract, chiefly 
in the dorsal region. 

The direct pyramidal tract of the right side is also affected in the three upper sections. 

of the knee-jerk) is seemingly regulated as follows : If, in the 
lumbar and lower dorsal region, the zone of entry of the 
posterior nerve-roots {vide p. 28, footnote) is sclerosed, then 
the knee-jerk is lost, however great the lateral sclerosis ; if, 
however, this part is healthy, the knee-jerk remains, and is 
even exaggerated, owing to the lateral sclerosis. 



224 NERVOUS DISEASES. 

The commonest form of postero-lateral sclerosis appears 
to be that in which the gait is partly unsteady, partly 
dragging, and the tendon-reactions are excessive ; sen- 
sory symptoms, and particularly lightning pains, are slight 
or absent ; the pupils act normally, or are occasionally 
of the Argyll-Robertson type ; a history of syphilis is less 
frequent, according to Dr. Gowers, than in uncomplicated 
tabes. 

In addition to the degeneration of the posterior columns 
and of the pyramidal tracts, the cerebellar and antero-lateral 
tracts (one or both) may be diseased ; so that there is a 
combined sclerosis of several systems of fibres. The degener- 
ation of these tracts makes no difference to the symptoms, so 
far as we know. Or it may be that the lines of the disease do 
not completely identify themselves with the systems of fibres, 
as known to us. 

A combined sclerosis is not un frequent in the spinal cords 
of general paralytics. 

Hereditary Ataxia, or Friedreich's Disease. — There 
is a form of ataxia which differs in several ways from ordinary 
tabes. It generally occurs (unlike tabes) in several members 
of a family ; mostly in collateral members — brothers and 
sisters, or cousins — sometimes among the ancestry too. It 
attacks the patients during youth, or even during childhood. 
The earliest symptoms are not, as in tabes, pains or anomalous 
paralyses, but a simple progressive inco-ordination of the 
lower limbs, trunks, arms. There are unsteady, irregular move- 
ments and swayings, which may look like mild chorea. The 
gait is unsteady and lurching. The tendon-reactions, as in 
tabes, are almost always abolished. The pupils, on the other 
hand, are quite normal. 

As the disease progresses other phenomena develop. The 
speech becomes peculiar, blurred and drawling, with elision 
of syllables. Nystagmus appears, though often not till late. 
The spinal column becomes curved, the foot becomes humpy- 



DISSEMINATED SCLEROSIS. 225 

looking, and the toes turn up. The lower limbs, from being 
simply ataxic, become actually weak, and a certain amount of 
rigidity may develop. The face becomes expressionless and 
feeble-looking, even though intelligence is unimpaired. The 
disease is slowly progressive ; and probably most cases are 
terminated by intercurrent disorders. Acute specific diseases 
appear to have a particularly deleterious effect on such patients. 
Not many cases have been investigated post-mortem, but it 
would appear from them that the disease consists in a "com- 
bined system degeneration," in which the posterior sclerosis 
forms the earliest and most completely developed factor. 
Hence the rule that the tendon-reactions are abolished, but in 
some very rare cases, they may be retained or even exag- 
gerated. 

Disseminated or Insular Sclerosis, " Sclerose en 
Plaques." — Disseminated sclerosis is a disease that affects 
the brain, and sometimes the nerve-trunks, as well as the cord. 
But since spinal symptoms are almost always present, and since 
they contrast in many ways with those of tabes, we shall 
consider it here. Anatomically, it is a "diffuse" lesion, 
characterized by the presence of islets or patches of disease 
irregularly scattered through the nervous system, and involving 
indiscriminately the various tracts and systems of gray or 
white matter. These patches are dull pink, translucent, and 
raised, or gray and contracted, according as they are recent or 
old. Within these patches there is an overgrowth of neuroglia 
and degeneration of nerve-tissue. As the neuroglia becomes 
thickened, and gradually converted into a fibrillar mesh-work, 
so does the myeline of the white fibres perish and become 
absorbed. The axis cylinders, according to most authorities, 
become at first enlarged ; later on they may perish, but, as a 
rule, some of them are said to persist even in patches of 
advanced sclerosis. This persistence of the axis cylinders has 
been used to explain another fact — viz., that secondary degen- 
eration does not take place with the same regularity as in 



226 NERVOUS DISEASES. 

other forms of myelitis. (Thus, when a patch of disseminated 
sclerosis involves the whole area, say of the cervical region, 
we may still find the pyramidal tracts healthy at a lower level 
of the cord.) When the disease affects the gray matter there 
may be degeneration of the ganglion-cells, but these, too, 





Fig. 60. 






Cervical 


Dorsal 


Lumbar 


Sacral 


region. 


region. 


region. 


region. 




© CD 



Disseminated Sclerosis of the Spinal Cord. 

appear able to hold out in the presence of considerable 
disease in their neighborhood. 

Little is known as to its causation. Unlike tabes, it affects 
women oftener than men, and commences comparatively early 
in life, usually before thirty. Exposure to cold, injury, acute 
infectious diseases, etc., have been observed to precede its 



DISSEMINATED SCLEROSIS. 227 

attack ; and still more frequently mental factors, such as 
fright, anxiety and worry, chagrin and disappointments. 
Syphilis has no relation to this disease. 

Typical Case. — A classical case of disseminated sclerosis 
presents a sufficiently characteristic picture. The patient is 
most frequently a women of middle age, or younger. Her 
aspect may be vacant and fatuous, and her behavior suggests 
that she is hysterical. The chief complaint is loss of power in 
the legs, and on examination this paraplegia is found to be of 
the "spastic" type; i.e., there is more or less rigidity, 
increase of tendon-reactions, and probably ankle-clonus. 
Sensation may or may not be affected ; the same may be said 
of the functions of the bladder and the rectum. When she 
attempts to use her hands a tremor seizes them, consisting of 
coarse, imperfectly rhythmical movements, which cease again 
when the hand comes to rest. A cup of fluid gets spilt as she 
lifts it to her lips. When she rises to walk similar movements 
may attack the head, trunk, and legs. Tremulous movements 
of the eyeballs are seen (" nystagmus ") as she fixes or follows 
an object. Her speech is peculiar. It is usually described 
as "scanning" — that is, the words and syllables, instead of 
having their proper flow, are brought out in a staccato fashion 
with an undue break between them. 

The history which has led up to this condition may differ 
much in different cases. Some of the following factors may 
very likely figure in it : repeated attacks of vertigo ; attacks 
of coma suggestive of cerebral hemorrhage ; transitory 
paralysis of one limb ; or, still more frequently, numbness or 
loss of sensation in various parts of the body and limbs, which 
has also passed away ; ocular paralysis, and temporary blind- 
ness. After these premonitory symptoms, or along with them, 
the paraplegia has gradually and permanently developed. 

The prognosis, when the disease is well established, is not 
good. Probably the paraplegia will become absolute, and the 
contractures of the legs extreme, and the patient, thoroughly 



228 NERVOUS DISEASES. 

bed-ridden, will die of cystitis, bedsores, or intercurrent 
disease. Or bulbar symptoms may supervene, and dyspnoea 
or difficulty of deglutition may prove fatal. Or she may die 
in one of the apoplectic attacks, to which we have alluded. 
But it is important to know, on the other hand, that the 
course of the disease may be interrupted by remissions of the 
symptoms so complete as to suggest a cure. Such remissions 
have even been observed to last two or three years. Their 
occurrence must make us feel uncertain of prognosis and 
diagnosis too. 

We know of no remedy as yet that can be relied on to 
cure this disease. 

Anomalous Cases. — The diagnosis of disseminated 
sclerosis where it does not conform to, or has not yet devel- 
oped into, the type we have sketched above, is a matter of 
great difficulty. The islets of disease may be placed any- 
where, and hence the symptoms (even such as are directly 
dependent upon the organic lesions) may be various and 
variously grouped. The tremor, the nystagmus, and the 
affection of speech are perhaps the most characteristic symp- 
toms, and it is for these especially that we should look out in 
doubtful cases. But they may appear only at a late period, 
or not at all. The condition of the eyes deserves study. 
Nystagmus, as we said, is common here. If we except 
Friedreich's ataxia, certain cases of peripheral neuritis, and 
growths in the upper part of the pons which gradually affect 
the ocular nuclei and nerve roots, it is an uncommon symptom 
in other nervous diseases. Paralysis of ocular movements 
occur both in this disease and in tabes ; Charcot affirms that 
in tabes such paralyses generally have the character of nerve- 
trunk paralysis, in disseminated sclerosis that of nuclear 
paralysis ; in other words, they are paralyses of conjugate 
movements (vide p. 128). As to the pupils, they act nor- 
mally, as a rule, to light and accommodation, unlike the 
pupils of tabes. Affections of vision occur which are rather 



DISSEMINATED SCLEROSIS. 229 

puzzling. The sight of one eye may be impaired and 
perhaps regained again, without any definite ophthalmoscopic 
change being seen ; or there may be optic atrophy of various 
degrees. Such atrophy, however, is not necessarily progres- 
sive, as in tabes ; in fact, there are very few cases recorded 
where total blindness has resulted from this cause. In some 
rare instances optic neuritis has been observed. 

The symptoms may be so scanty, while the disease is yet 
developing, as to make a definite diagnosis almost impossible. 
There may be little more than paraplegia, indistinguishable 
from that of chronic myelitis, or from hysterical paralysis. 
Hemiplegia may be the leading symptom ; this may be of 
several kinds : either a hemiplegic tremor or a transient 
hemiplegia following a quasi-apoplectic seizure, or a perma- 
nent hemiplegia which is chiefly remarkable by its gradual 
onset. Or the disease may begin with inco-ordination of 
gait and lightning pains, or gastric crises, like those of tabes. 
Ataxy with paresis of the lower limbs, affection of speech, 
and nystagmus, are symptoms which may be found both in 
this disease and in Friedreich's ataxy ; but in the latter dis- 
ease the tendon-reactions are usually abolished, and the 
symptoms are developed in a more definite course. Nystag- 
mus, with paralysis of ocular movements, tremors, and weak- 
ness of the limbs, coupled with exaggeration of tendon- 
reactions, and possibly some difficulty of speech, may be 
seen in tumors high up in the pons as well as in disseminated 
sclerosis. But the commonest difficulty that arises is the 
distinction between hysterical paralysis and disseminated 
sclerosis, by reason of the age, sex, and general character of 
the patients, and the anomalous grouping and course of the 
symptoms, which may be much the same in both affections. 
Two additional statements may be made here, which will set 
forth this difficulty still more strikingly : first, that, according 
to Charcot, sclerosis may become engrafted upon long-con- 
tinued hysterical disease ; secondly, that, according to West- 
20 



23O NERVOUS DISEASES. 

phal, cases occur indistinguishable during life from dissemi- 
nated sclerosis, and actually proving fatal, wherein after death 
no trace of organic lesion can be found. 

General Paralysis of the Insane, or Paralytic De- 
mentia. — General paralysis is a disease which affects both 
the cortex cerebri and the spinal cord. We shall notice it 
here, partly for the sake of comparison with the other degen- 
erative diseases of the spinal cord, partly because the general 
physician has chiefly to do with it in the form of a spinal dis- 
ease, or at least with that variety of it in which mental symp- 
toms are inconspicuous. Like tabes dorsalis, it is much more 
common in men than in women. Overwork, the anxieties of 
business, over-indulgence in alcohol or in sexual intercourse, 
injuries to the head, are alleged causes. Syphilis, even if it 
do not produce the true disease, may be followed by a con- 
dition closely resembling general paralysis. 

The condition of the brain in an advanced case of general 
paralysis has been thus described. The dura mater (and per- 
haps even the bones of the skull) is thickened. Beneath the 
dura are sometimes found exudations which have the appear- 
ance of a blood-clot. The arachnoid is milky and opaque : 
there is much sub-arachnoid fluid. The convolutions them- 
selves are shrunken ; the pia is tough, and when peeled off 
takes with it part of the surface of the convolutions, so that 
they have an eroded appearance. The lining membrane of 
the ventricles is rough and thickened. The gray matter of 
the convolutions is thinned, and shows an opaque outer layer 
with a line of congestion beneath. The minute changes ap- 
pear to consist in an overgrowth of the neuroglia, and atrophy 
of the cells and nerve-fibres of the gray matter. Probably 
general paralysis should be regarded as a primary disease of 
the brain substance ; but good authorities maintain that the 
disease originates in the vessels, and that the nervous changes 
are secondary to repeated congestion. In the spinal cord 
there may be degenerations, like those we have been con- 



GENERAL PARALYSIS. 23 I 

sidering, either of the pyramidal tracts or of the posterior 
columns. 

Mental Symptoms. — The most typical cases of the dis- 
ease exhibit a combination of mental and bodily symptoms 
from which has originated the name "general paralysis of the 
insane." The insanity will most likely manifest itself in 
some such ways as these : The patient's habits and character 
undergo a change ; he becomes careless and incapable in busi- 
ness matters, and at home egotistical, conceited, extravagant, 
perhaps immoral. He may embark in all sorts of foolish 
schemes and expenditures before it is recognized that he is 
mad. Then actual delusions appear, of the " expansive" or 
grandiose character. He has millions of money, hundreds of 
wives, and has the strength of many men, etc. He will 
ramble on in his talk from one scheme to another, or will 
hurry hither and thither in pursuit of imaginary business. He 
is not violent, as a rule, unless thwarted or contradicted. 
After some time this state of exaltation begins to give way to 
a state of stupid contentment, though the patient will still be 
found to have delusions when questioned. The paralytic 
symptoms have also in the meantime been making way. 
Finally, he will lapse into complete dementia, and mind and 
body alike failing, he will die, probably in some three or four 
years from the commencement of his illness. 

Physical Symptoms. — Bodily symptoms accompany 
these mental changes, and they are important to recognize ; 
for there is a large class of cases in which the delusions and 
mania do not develop. Such patients are not lunatics, but, 
equally with those who are, they undergo a process of mental 
enfeeblement, and end in the same state of "paralytic de- 
mentia." 

One of the most characteristic and earliest physical symp- 
toms relates to the speech. As the patient begins a sentence 
he hesitates slightly, and there are fine tremulous movements 
of the lips. Towards the end of a long and difficult sentence 



232 NERVOUS DISEASES. 

or word he slurs the syllables and perhaps drops some out. 
"National Hospital for the Paralyzed and Epileptic" be- 
comes " N-national Hospital for the Parlyzed and Etlettic." 
The speech differs therefore from the "scanning" of dissemi- 
nated sclerosis, and from the drawl of patients with right 
hemiplegia ; in later stages, however, the general paralytic 
lapses into a mere drawl. Usually when he shows his teeth 
or puts his tongue out, his lips and tongue will shake, perhaps 
very much. His hands shake as he uses them ; but it is a fine 
tremor, not the coarse vibration of disseminated sclerosis. 
There is a feebleness of the limbs, and it is generally for this 
that the patient (when not mentally affected) seeks advice. 
It will be found on examination either that there is mere 
motor weakness with exaggeration of tendon-reactions, or that 
there is an ataxic condition with absence of tendon-reactions, 
or that these two states are more or less combined. These 
facts stand in relation to the presence of lateral or posterior 
sclerosis, or combined postero-lateral sclerosis — all of which 
have been found in the spinal cord post-mortem. As to 
the eyes, there is no nystagmus, and the ocular movements 
are normal ; but the pupils may be unequal, and they often 
exhibit reflex iridoplegia, contracting under light but not to 
accommodation. Optic atrophy may occur, but it is not very 
common. It is obvious that an ataxic gait, with absence of 
tendon-reactions, and pupils of the type just mentioned, will 
suggest the diagnosis of tabes dorsalis, but general paralysis 
should be suspected where there is mental enfeeblement, where 
the speech is affected, where the ataxia or feebleness has devel- 
oped rapidly, and where there has been an absence of lightning 
pains. Nevertheless, though the two diseases must be distin- 
guished, they have evidently a close relation to each other. 
For, as the general paralytic may have symptoms of tabes, and 
actual posterior sclerosis, so may the patient who for many 
years has had tabes, develop the mental and bodily symptoms 
of general paralysis {vide p. 220). Another set of symptoms 



MUSCULAR ATROPHY. 233 

remains to be noticed ; they often occur early in general 
paralysis and are always of importance. These are the so- 
called "congestive" attacks. The patient may become sud- 
denly comatose, as if from cerebral hemorrhage. Or he may be 
attacked with convulsions, either general convulsions rapidly 
repeated, constituting a "status epilepticus " (vide "Epi- 
lepsy"), or convulsions limited to one arm, leg, or one side 
of the body. Or he may become for a time hemiplegic, with 
or without convulsions or coma. Such symptoms may occur 
indeed in any degenerative nervous disease (we have already 
noticed their possible occurrence in disseminated sclerosis), 
but they are particularly frequent in general paralysis. Such 
attacks usually leave the patient worse in every way ; or he 
may die in them. Indeed, it is said that a fatal attack of this 
nature may be the very first symptom of the disease. 

General paralysis is a very fatal disease, usually terminating 
within three or four years from its commencement. The 
course of those cases where the delusions are predominant can 
evidently be watched only in asylums, and for a full descrip- 
tion of them we must refer to text-books on lunacy. It is 
important to be aware of the existence of the other class of 
cases, which show themselves simply by progressive paralysis 
and mental enfeeblement, partly because delusions may at any 
time appear, partly because the fatal termination is the same. 
Nevertheless, there may be remissions in some cases, and 
others may run an abnormally slow course. We know of no 
drugs that will cure the disease ; though, where it can be 
connected with syphilis, iodide of potassium in large doses 
has appeared to do good. 

Progressive Muscular Atrophies. — Muscular atrophy 
is a symptom that occurs in many nervous diseases. In its 
most marked form, it indicates a lesion of the lowest parts of 
the motor tract — that is to say, either the large cells of the 
anterior cornua, or the nerves that connect these cells with 
their muscles, or the muscles themselves. Disease of the 



234 NERVOUS DISEASES. 

motor apparatus above the level of these cells — viz., of the 
cerebrum and pyramidal tracts — causes, as a broad rule, 
not muscular wasting, but the opposite phenomenon, mus- 
cular rigidity. (With the anterior cornual cells of the cord 
we include their homologues, the motor nuclei of the me- 
dulla.) 

Under the heads of infantile spinal paralysis (acute anterior 
cornual myelitis), diffuse myelitis, and neuritis, we have 
described the diseases which commonly are the cause of acute 
muscular atrophy ; we have now to describe some diseases in 
which the chief symptom is a chronic and progressive atrophy. 
Some of these undoubtedly have their primary seat in the 
spinal cord, others in the muscular tissue itself, some perhaps 
in the nerves. 

Amyo-trophic Lateral Sclerosis (Charcot's type). 
— Amyo-trophic lateral sclerosis is the name given by Charcot 
to a disease characterized anatomically by two main factors — 
degeneration of the white fibres forming the pyramidal tracts, 
and degeneration of the anterior cornual cells. The clinical 
correlatives of these anatomical factors are spastic paralysis, 
and paralysis with atrophy of muscle. Let us consider a 
typical case. The age of the patient, who may be man or 
woman, ranges usually from twenty-five to fifty years. The 
first symptom is weakness of the hands. This may be accom- 
panied by numbness, or other disagreeable sensations, or even 
by distinct pains, but such sensory phenomena are not marked 
nor permanent. Soon the intrinsic muscles of the hands are 
found to be wasting; then the forearms become small, flabby, 
and waste also. The weakness and wasting thus spread 
through the whole upper limbs. If we examine the patient at 
a comparatively early stage, we shall probably find the fol- 
lowing condition : marked wasting of hand-muscles, fore- 
arms small and flabby if not wasted, indications of weakness 
and atony in the upper-arm and scapular muscles. The 
muscles which are beginning to waste show well-marked 



MUSCULAR ATROPHY. 235 

intermittent twitchings of their muscular bundles (fascicular 
tremors, vide -p. 103). 

Electrical examination generally shows, in muscles where 
the wasting is declared but not extreme, an incomplete reac- 
tion of degeneration — i.e., farado-contractility retained, but 
galvanic formula, and perhaps character of the muscle twitch, 
altered. But in some muscles the reactions may be normal, 
and in extremely wasted muscles the electro-contractility may 
have disappeared. Lastly, and this is most important, this 
atrophic paralysis is accompanied by increase in the tendon- 
reactions. This exaggeration may be observed in the arms, 
provided the wasting has not advanced too far ; and still 
better in the legs, even before the patient complains of weak- 
ness here. It is, in fact, the herald of the second stage of 
the disease. 

This second stage is marked by the access of paraplegia. 
The paraplegia is at first due to the lateral sclerosis, and is 
therefore of the spastic type. The feet are dragged in walking, 
there is increased knee-jerk and probably ankle-clonus. There 
is no sensory paralysis and no paralysis of the sphincters ; no 
bedsores. But there will not be an extreme degree of rigidity, 
for the reason that before the lateral sclerosis had had time 
to become extreme, degeneration of the motor cells will begin 
in the lumbar enlargement, introducing the opposed con- 
dition of flaccidity. Thus there is found in the lower limbs 
first rigidity more or less, then a kind of compromise which 
has been called " flexibilitas cerea " ; lastly, flaccidity and 
atrophy, as in the arms. 

In the third stage, the disease attacks the bulbar nuclei. 
Nasal voice, progressive difficulty of articulation and of 
swallowing are the usual symptoms. Wasting and fibrillary 
twitchings are seen in the tongue, the palate moves badly, the 
lower part of the face becomes expressionless. Extension of 
the disease to the respiratory and cardiac centres may ob- 
viously induce fatal attacks of dyspnoea and of syncope, if 



236 NERVOUS DISEASES. 

the patient have already survived his state of paralysis and 
mal-nutrition, with its risks from intercurrent disorders. 

The causes of the disease are practically unknown. The 
prognosis is bad, for the progress is more rapid than that of 
most spinal degenerations, and death results within three or 
four years, although exceptional cases may run a longer course. 

A typical case is easy to recognize, but there are varieties. 
Thus some cases begin with bulbar symptoms, such as paralysis 
and wasting of the tongue ; sometimes the weakness is for a 
time predominant in the arm and leg of one side, so as to bear 
a rough resemblance to cerebral hemiplegia ; sometimes the 
paralysis of the legs may be atrophic from the first. It 
would appear, indeed, that a certain class of cases, in which 
post-mortem degeneration of the anterior cornual cells is 
found coupled with lateral sclerosis, and which therefore cor- 
respond anatomically to amyo-trophic lateral sclerosis, do 
not exhibit spastic phenomena during life. The explanation 
presumably is that the cells are attacked before the pyramidal 
fibres. This occurs particularly when the disease begins in 
the bulbar nuclei. The case then exhibits paralysis with 
wasting of the tongue, paralysis of the lips and lower face, 
of the palate, and it may be of the larynx. As the disease 
advances, atrophy of the hand-muscles, shoulder-muscles and 
other parts begins. This has been called " progressive bulbar 
paralysis." 

The morbid anatomy consists in a degeneration of the 
anterior cornual cells and of the pyramidal tracts. There is 
disease also of the motor nerves and of the muscles, partly 
secondary to that of the motor cells, partly it may be primary. 
The disease in the pyramidal tracts has been traced up into 
the crura cerebri, and in a few instances beyond this — viz., 
through the internal capsule and corona radiata, even into the 
motor convolutions. 

Chronic Degeneration of Anterior Cornual Cells 
(type Aran-Duchenne). — In the second form of pro- 



MUSCULAR ATROPHY. 237 

gressive muscular atrophy, which is dependent upon spinal 
disease, sometimes known as the " type Aran-Duchenne," the 
degeneration is limited to the anterior cornual cells, the 
lateral columns not being affected.* Probably this form is 
much less common than was formerly thought. It is distin- 
guished from amyo-trophic lateral sclerosis by the following 
features : — 

There are no spastic phenomena, so that the legs are not 
stiff nor the tendon-reactions exaggerated. 

The wasting begins in the hands, but its method of exten- 
sion is different. Instead of involving several adjacent muscles 
rapidly and en masse (as does amyo-trophic lateral sclerosis), 
it picks out muscles and even parts of a muscle, one by one, 
and that slowly, so that it may remain for a long time localized 
in a few muscles. 

There are involuntary muscular twitchings, but of quite 
small tracts of fibres (fibrillary tremors.) 

The paralysis does not precede or outrun the muscular 
atrophy as in amyo-trophic lateral sclerosis, but it is propor- 
tionate to it. (Similarly it is said that, electrically, the 
muscular reaction becomes simply deficient in proportion as 
the muscle wastes, but it is probable that qualitative changes 
will be found with the galvanic current, if carefully looked 
for. ) 

The disease proceeds very slowly and may last for years. 
The patient may be reduced to a mere skeleton ere death 
ensues, from respiratory complications, or from spread of the 
disease to the medulla. 

Peroneal Type. — A third form has recently been isolated 
from the group of muscular atrophies, which has the following 



*Some authors maintain that the lateral columns become affected sooner 
or later in all forms of spinal amyo-trophy. In that case the anatomical 
distinction between this disease and amyo-trophic lateral sclerosis breaks 
down. But the clinical types are certainly distinct, though there are (as 
we have indicated in the text) sundry intermediary forms. 



238 NERVOUS DISEASES. 

characteristics. It commences in the muscles of the lower 
leg, most commonly the peroneal group. From this circum- 
stance it has been called the peroneal type of muscular 
atrophy (Howard Tooth). Thus, a club-foot is often the 
first symptom. The two legs are affected either simultane- 
ously, or one shortly after the other. As time goes on, all 
the muscles below the knees are attacked, so that the leg looks 
shapeless and thinned. The skin may become cold and blue. 
As the patient is frequently a child, this condition is readily 
mistaken for a late stage of acute anterior cornual myelitis, 
unless attention be paid to the history, which is that of gradual 
onset. The thigh-muscles appear able to hold out against 
the disease for a long time, and while they do so the patellar 
tendon-reaction is retained. Later, it may be some two or 
three years later than the legs, the intrinsic muscles of the 
hands begin to waste, and after them the muscles of the fore- 
arms become thinned, like those of the legs. From the most 
deeply affected muscles electro-contractility may have disap- 
peared, in others reaction of degeneration, in various stages 
of completeness, has been discovered. A remarkable fact 
concerning this type of atrophy is that it often affects brothers 
and sisters of one family, and occasionally (it would seem) 
members of succeeding generations ; in this it resembles the 
disease we shall next describe. Concerning its course and 
ultimate conclusion, we have yet much to learn ; we only 
know that it spreads very slowly. The morbid anatomy is as 
yet uncertain ; most authorities believe it to be a form of 
neuritis. If this be so, it explains the facts noted by Charcot 
and Marie, that in some cases there are pains and even an- 
aesthesia of the legs and soles. 

Myopathic Types (Erb). — The remaining forms of 
progressive atrophy are considered to be due neither to dis- 
ease of the cord nor of the nerves, but of the muscle substance 
itself; hence they are sometimes called "myopathic" atro- 
phies, or "muscular dystrophies." There is a form which 



MUSCULAR ATROPHY. 239 

begins in early adult life (usually before twenty), or less com- 
monly in childhood, and which has therefore been called 
"juvenile muscular atrophy." It begins, not like the spinal 
atrophies, in the small muscles of the hands, but in the larger 
muscles which move the scapula and shoulder-joint, trapezius, 
pectoralis serratus, etc., or those of the upper arm. The del- 
toid is often intact (or even enlarged).* The erectores spinse 
are often weak, and the muscles which pass from the pelvis to 
the thigh suffer. In some cases the calf-muscles may be en- 
larged and hard. Even the atrophied muscles have not the 
flaccid feel of true spinal amyo-trophy ; and electrical testing 
shows that, though their contractility may be diminished to 
both currents, there is no reaction of degeneration. Neither 
do the muscles show fibrillary or fascicular twitchings.f There 
are no spastic symptoms ; the knee-jerks are never exagger- 
ated ; indeed, they gradually diminish and disappear. Such 
disappearance is due, not to lesion of the nervous arc, but to 
invasion of the quadriceps extensor cruris by the disease. 
Bulbar symptoms do not develop. As in the peroneal type, 
there is <3ften a family proclivity to the disease. The course 
of the disease is slow, and may be interrupted by long sta- 
tionary periods. 

There is a variety of this form, distinguished as follows : it 
begins in childhood (hence sometimes called " infantile"), and 
the muscles of the face are affected from the first. At first 
sight the facial palsy is not very obvious. The lips are thick, 
somewhat everted and protruding ; both lower face and fore- 
head are expressionless, and move little, if at all, on 
laughing, etc. ; the eyes cannot be completely closed. The 
large muscles of the shoulder girdle and limbs atrophy later. 



* If, as may be the case, the deltoid remains intact while the spinati and 
flexor muscles of the elbow are atrophied, this in itself suggests that the 
lesion is not spinal, since the nuclei for these muscles lie near together. 

f These statements hold good for most myopathic cases, but are perhaps 
not of universal application. 



240 NERVOUS DISEASES. 

It would appear, from such examinations as have been made 
of these forms of muscular atrophy, that the spinal cord and 
nerve are free from disease, but that the muscular tissue shows 
some changes as follows : simple atrophy of some fibres, 
perhaps hypertrophy of others, longitudinal splitting of 
fibres ; multiplication of the muscular nuclei, sometimes to 
such an extent that they invade and disorganize the muscle 
substance; sometimes vacuolization of muscle fibres; over- 
growth of the interstitial tissue with multiplication of its 
nuclei; infiltration of the interstitial tissue with fat in some 
extreme cases. 

Pseudo-hypertrophic Paralysis. — In pseudo-hyper- 
trophic muscular paralysis the muscles (or at least some of 
them) appear enlarged and feel unduly firm, but nevertheless 
are weakened. The anatomical changes in them consist, 
according to Dr. Gowers, of an overgrowth of fatty tissue, 
or it may be merely of connective tissue in the interstices 
between the muscular fibres, with simple atrophy or perhaps 
degeneration from pressure of these fibres. There may be no 
disease in the spinal cord. It is a disease that begins in child- 
hood, as a rule, about five or six years of age ; though even 
before this, lateness in learning to walk, or even unsteadiness 
upon the feet, may have been observed. It is apt to run in 
families, and males are often more affected than females, 
though the disease is transmitted through the female. The 
calf-muscles are those in which enlargement shows itself 
most strikingly and constantly ; the muscles of the thigh, 
the glutaei of the upper arm, and (very frequently indeed) 
the infra-spinatus, may also be enlarged. Other muscles may 
be small or congenitally absent, particularly the pectoralis 
major and latissimus dorsi ; and in course of time the enlarged 
muscles may waste. The muscular weakness produces certain 
peculiar symptoms. In walking, the patient keeps his trunk 
thrown backward, because his erectores spina? are weak ; and 
his trunk oscillates from side to side with each step, because 



PSEUDO-HYPERTROPHIC PARALYSIS. 24 1 

his glutsei medii are weak and balance it ineffectively. He may 
be unable to walk up stairs. If put on the floor in the prone 
position and told to rise, he first pushes himself off from the 
floor by his hands, and, after he has thus half raised himself, 
completes the action by placing his hands on his thighs, and 
so gradually pushing himself into the erect position. Lateral 
curvature of the spine often ensues from weakness of the 
muscles. Club-foot may be produced from gradual con- 
traction of the paralyzed muscles. The patellar tendon-re- 
action disappears as the extensors of the knee lose power. 
Electrically there is gradual diminution of contractility, with- 
out reaction of degeneration. 

As the disease progresses, the patient becomes quite unable 
to walk, and finally even to sit up. Death usually comes from 
intercurrent disease, especially upon the side of the lungs, 
usually between twelve and twenty years of age, according to 
Dr. Gowers, except in cases where the symptoms have shown 
themselves at a later age than usual, when the progress is often 
much slower. The same author insists on the importance of 
keeping the patient as long as possible from becoming bed- 
ridden, partly because muscular exercise appears to retard the 
disease, partly because deformities from contracture make more 
rapid progress when he is once laid up. Courses of gym- 
nastics, massage, and judicious tenotomies he recommends 
with the view of retarding the disease. 

The close relation between this and the myopathic form of 
muscular atrophy is evident from the following considera- 
tions : In this disease there is apparent hypertrophy of some 
muscles, with deficiency of others ; in that, atrophy of some 
muscles with (sometimes) hypertrophy of others; in both, the 
cord is unaffected ; in both, the electrical conditions of the 
muscles and the condition of the tendon-reactions are the 
same; in both there is often found a family proclivity to the 
disease. Lastly, intermediate cases are known of which pro- 
gressive weakness of muscle (the common feature of the two 



242 NERVOUS DISEASES. 

diseases), without either atrophy or hypertrophy, has been 
the only characteristic. Indeed, by some authors, pseudo- 
hypertrophic paralysis and myopathic atrophy are considered 
to be essentially the same disease. 

Thomsen's Disease, " Myotonia Congenita." — 
Thomsen's disease is a rare affection of the muscular system 
which, like those we have just been considering, runs in fami- 
lies, and develops early in life, sometimes quite in infancy. Its 
principal feature is this, that when the patient begins a volun- 
tary movement, the muscles are thrown into a condition of 
spasm, which interferes with the movement, or may even 
temporarily fix him to one position. This phenomenon takes 
place only at the commencement of movement, and generally 
passes off in a few seconds. Naturally it is best shown in the 
muscles of the limbs, but those of the face, tongue, and eyes 
may be affected also. Curious effects may be produced where 
the spasm is extreme ; thus one patient in mounting a horse 
had to stand with one foot in the stirrup before he could get 
the other foot off the ground ; a second patient had attempted 
to strike another man, but was held fast by the spasm till his 
adversary knocked him down. Usually, however, a mere 
stiffness and awkwardness of movement is caused. The mus- 
cles are often enlarged, and firm to touch, but they are not 
strong in proportion to their enlargement. The effect of a 
blow on the muscle is to produce, not a transient contraction 
as in health, but a tonic contraction, lasting several seconds, 
of the fibres which have been struck. Similarly, electrical 
stimulation of the muscle produces a tonic contraction, 
instead of a single spasm, in response to each shock. This is 
best seen with the constant current. Further, according to 
Erb, the application of a strong constant current without 
make or break produces certain rhythmical wave-like mus- 
cular contractions, which proceed from the area of the 
kathode to that of the anode. The tendon-reactions are 
normal, or in some cases absent. The peculiar muscular 



MUSCULAR ATROPHY. 243 

spasm is aggravated by cold, by anxiety to hurry, and by the 
knowledge that other persons are observing it. The disease 
does not appear to endanger life or health, but only to cause 
inconvenience. No post-mortems have yet been made ; but 
in excised pieces of muscle Erb has found hypertrophy of 
muscle-fibres with increase in the number of nuclei. 

Some General Remarks on the Group of Muscular 
Atrophies. — Before returning to diseases of the cord and its 
membranes, from which we have unavoidably digressed, 
some general remarks may be made on the forms of muscular 
atrophy which we have described. Their classification into 
clinical types is based, it will have been noticed, on observa- 
tion of the following points : — 

1. Where does the atrophy begin, in the small muscles of 
the hand, large muscles of shoulders or pelvic girdle, facial 
muscles, or leg muscles ? 

2. How does it subsequently spread, piecemeal or whole- 
sale ? with a distribution that suggests a spinal origin, or that 
is irrespective of this ? 

3. What is the physical condition of the muscles — i. e., do 
they show fibrillary twitching or not ? are they flabby or 
firm ? is there electrical reaction of degeneration or not ? is 
the paralysis proportionate to the atrophy or in excess of it ? 

4. Are other nervous phenomena present besides muscular 
atrophy of the limbs, such as sensory affections, rigidity, and 
excess of tendon-reactions, bulbar symptoms? 

5. What is the age of the patient at the onset? is there a 
family proclivity to the disease ? what is the rate at which the 
disease progresses ? 

The clinical types correspond fairly well with distinctions 
in morbid anatomy; thus in the type of Aran-Duchenne there 
is disease of the spinal motor-cells, in amyo-trophic lateral 
sclerosis disease of the spinal motor-fibres as well, in other 
forms disease of the muscles, in the peroneal type probably 
disease of the nerves. 



244 NERVOUS DISEASES. 

Nevertheless they all have this in common, that they are 
degenerations of the motor system of nerve and muscle, 
though they may differ in the point which they attack and 
the course which they take. It is not surprising if such differ- 
ences are not always uniform. And thus we find that in cases 
which correspond mainly to the " myopathic " type — i.e., 
to primary disease of the muscle, features are sometimes found 
which are ordinarily thought to be distinctive of spinal disease 
— viz., fibrillary twitching and reaction of degeneration. And 
if we turn to morbid anatomy, we see that amyo-trophic 
lateral sclerosis (the form of muscular atrophy whereof the 
morbid anatomy is best known) may begin sometimes in 
the pyramidal tracts, sometimes in the spinal motor-cells, 
sometimes in those of the medulla, and that eventually it may 
involve the whole motor tract, from cortex cerebri to the 
muscles inclusive. Here therefore we have a degeneration of 
the motor system which may vary in its point of attack, or 
may perhaps attack more than one point, and which becomes 
rapidly generalized ; in the other types we have less intense 
and more local degenerations, which exhibit, each of them, 
features that differentiate them broadly, but that do not abso- 
lutely and widely separate them. 

Treatment may do good, but cannot be relied upon to 
produce an absolute arrest or cure. It is doubtful whether 
anything can be done to stop the march of amyo-trophic 
lateral sclerosis. The other forms of muscular atrophy are 
usually treated by massage and galvanism : as drugs, strychnia, 
arsenic, and iodide of potassium are given. Strychnia may 
also be injected into the wasting muscles. 

Arthritic Muscular Atrophy. — Atrophy of muscle may 
occur in connection with disease of joints. This is not simply 
the atrophy of disuse, for the joint disease may be slight (not 
incapacitating it for movement), and yet the atrophy be well 
marked. It is held to be due to a reflex irritation, started by 
the joint disease in the trophic spinal cells. Certain muscles 



SYPHILITIC AFFECTIONS OF THE CORD. 245 

are more readily affected than others ; thus, in disease of the 
shoulder-joint, the deltoid supra- and infra-spinatus waste, in 
disease of the hip the glutsei, in disease of the knee the quad- 
riceps, and generally the extensors (it is said) rather than the 
flexors. The tendon-reactions are often increased. There is 
no reaction of degeneration. The joint mischief must be 
rectified wherever this can be done ; the muscles rubbed, 
and strongish galvanism applied both to them and to the 
joint. As this form of atrophy is recoverable, or at least non- 
progressive, it is important to distinguish it from the more 
serious diseases that we have just been describing. 

We must now return to diseases of the cord and its mem- 
branes, to notice those which depend on other causes than 
simple inflammation, softening, or degeneration. 

Hemorrhage into the cord, unless as the result of inflam- 
mation, new growth, or injury, is so extremely rare that it 
need not detain us. Syphilis, tubercle, and new growths 
may affect the cord or its membranes. Of these tubercle 
usually occurs in the form of a meningitis, and tubercular 
spinal meningitis independently of cerebral meningitis, is not 
common. 

Syphilitic Affections of the Cord. — Syphilis affects 
the cord frequently and in several ways. 

(1) As a meningitis: this may be subacute and diffuse, as 
we have already said ; there will be probably less pain than 
in an acute general meningitis; the periphery of the cord 
itself is likely to suffer permanently. Or else the meningitis 
may be less acute and more localized. 

(2) Syphilitic arterial disease may lead to local softening ; 
should this occur (as it most often does) in the dorsal region, 
there will be simply a paraplegia of sudden onset, concerning 
the cause of which we can only conjecture. 

(3) Gummatous nodules may affect the nerve-roots, the 
membranes, or the cord itself; the nervous symptoms will point 
to gradually developing disease of these parts; the syphilitic 

21 



246 NERVOUS DISEASES. 

nature of them is inferred from general considerations, to 
which we shall recur when we discuss cerebral syphilis. 

A hemiparaplegia {vide p. 93) is very likely to be syphilitic, 
since it requires a small lesion limited to one side of the cord, 
and a gumma springing from the pia mater perhaps fulfils these 
conditions best. But even an ordinary paraplegia, where 
other causes can be fairly excluded, is not unlikely to be 
syphilitic, if we look merely to the comparative frequency of 
syphilitic nervous lesions. On the other hand, hereditary 
syphilis is said to affect the cord very rarely indeed. 

Tumors of the Cord and Membranes. — A new 
growth upon the spinal membranes produces at first symp- 
toms referable to the nerve-roots which it irritates or involves. 
These consist of sensory and motor irritation, followed by 
sensory and motor paralysis in the districts supplied by these 
roots. Thus, when the dorsal region of the cord is affected, 
the chief symptom will be pain around the trunk, easily mis- 
taken for pleurisy, rheumatism, intercostal neuralgia, etc. 
If the disease be opposite the cervical or lumbar enlargement 
there are pains in the limbs, and perhaps muscular spasms, 
followed by paralysis and wasting. In addition to such "ec- 
centric" pains, there may very likely be pain and tenderness 
at the seat of the disease. Afterwards, as the cord itself 
becomes damaged by the invasion or pressure of the growth, 
paraplegia with the other symptoms of tranverse myelitis fol- 
lows. We surmise that the disease is a new growth when such 
a train of symptoms has arisen without obvious cause, and 
advances steadily, uninfluenced by treatment (especially by 
antisyphilitic treatment, which should always be fully tried), 
and when caries of the vertebrae, syphilis, and other such 
sources of disease can be fairly excluded. 

New growths may also originate within the substance of the 
cord. These will give rise to the symptoms of a myelitis 
(paralysis with wasting of the muscles supplied from the 
affected part, followed by paralysis with rigidity of those sup- 



SYRINGOMYELIA. 247 

plied from the parts below) ; but these symptoms will have 
originated without apparent ca,use, and will have developed 
(in most cases) gradually, and will show signs of constant 
extension along the length of the cord. Moreover, the dis- 
ease is characterized by pains much more severe than in simple 
myelitis, and these not merely at points corresponding to the 
upper level of the disease (root pains), but in all the paralyzed 
limbs. Probably these pains are caused both by irritation of 
the intra-spinal nerve-roots, and by gradual spread of the 
growth to the membranes. 

It is needless to add that the diagnosis of intra-spinal tumor 
will be greatly aided by the presence of a new growth else- 
where, or by the history that such an one has been removed ; 
but more often than not the internal tumor stands alone. 
Nothing can be done medically for such a case, except to 
treat symptoms ; but a growth, capable of being accurately 
localized, and limited to the membranes, has been successfully 
removed by operation (Gowers and Horsley). 

Cavities in the Cord — Hydro-Myelia, Syringo- 
Myelia. — Dilatations of the central canal of the cord, or 
canals which have closed imperfectly, are occasionally found 
in the bodies of young subjects, without having given rise to 
any definite symptoms during life. To simple dilatations of 
the canal with fluid, the name hydro-myelia has been applied ; 
indicating the analogy of this spinal condition to the condi- 
tion of the cerebral ventricles known as hydrocephalus. 

In adults, the spinal cord sometimes exhibits a longitudinal 
cavity or cavities. This condition has been called "syringo- 
myelia " {syrinx, a pipe). There are two factors in syringo- 
myelia : (r) the longitudinal excavation of the cord; (2) the 
tissue which surrounds the excavation. The cavity, which is 
usually most marked in the cervical region, may either occupy 
the position of the normal central canal, or may be evidently 
distinct from it. In the latter case, it is usually placed in 
the posterior part of the cord, and therefore we are left in 



248 NERVOUS DISEASES. 

doubt whether it may not indicate an imperfection in the 
original formation of the central canal. (The normal canal 
is formed during development by the folding over, from 
before backward, of the tissues which are to constitute the 
cord ; and subsequent closing in of the gap left where these 
folds join.) These abnormal cavities may or may not have 
an epithelial lining. Outside this lining (if it exists) may 
come a firm but thin fibroid layer. Outside this again comes 
a formation of more importance. It appears to consist of an 
overgrowth of the neuroglia layer which normally surrounds 
the central canal ; this overgrowth may be so abundant as 
to cause considerable enlargement of the cord, and to consti- 
tute, in the opinion of some authors, a veritable new growth. 
It may be highly vascular, and exhibit hemorrhages into its 
substance. Opinions seem to differ as to whether an abnor- 
mal and dilated canal is the primary factor, and the growth 
of neuroglia around it secondary, or whether a new growth 
first forms and then breaks down in its centre, forming a lon- 
gitudinal cavity. 

These excavations in the cord have been considered, till 
recently, as mere pathological curiosities ; but it would appear 
that symptoms may be present which are more or less dis- 
tinctive of them. The train of symptoms depends not so 
much on the presence of a cavity, as on the fact that there is 
a progressive disease in the region of the gray matter (particu- 
larly its central or posterior parts) which reaches its maximum 
in the cervical region, and which may give rise to secondary 
degenerations of the white matter. Gradual loss of power in 
the upper limbs may attract the patient's attention ; in course 
of time muscular atrophy develops, doubtless because the 
anterior gray cornua are affected. But from the kinds of 
muscular atrophy we have hitherto considered, this disease is 
distinguished by its sensory abnormalities. The sense of 
touch and the muscular sense are preserved ; but the appre- 
ciation of temperature and the sensation of pain (one or both) 



SYRINGOMYELIA. 249 

are lost in many parts of the body. There are also nutri- 
tional disturbances (other than muscular atrophy) in the skin, 
in the nails, in the joints, in the secretion of sweat. Spon- 
taneous (and painless) ulcers and whitlows may form. Lat- 
eral curvature of the spine may develop : the reason for which 
is not obvious. In the lower limbs there is (in the later 
stages) paralysis with rigidity, due probably to descending 
degeneration in the lateral columns. Sometimes it is said 
the lower limbs are ataxic, and their tendon-reactions dis- 
appear. The course of the disease is slow, and there may be 
long periods of remission of the symptoms. On the other 
hand, sudden exacerbations may take place, which may pos- 
sibly be ascribed to the occurrence of hemorrhages into the 
newly formed gliomatous tissue. 



CHAPTER VII. 

ORGANIC CEREBRAL DISEASE. 

Symptoms. — We will nowbriefly enumerate the symptoms 
which point to intra-cranial disease: (i) those which are gen- 
eral ; (2) those which are referable to disease of particular 
parts of the brain, or as they are sometimes called, "localizing 
symptoms." 

(1) Of general symptoms, those which point most definitely 
to organic cerebral disease are — 

Paralysis, usually of the hemiplegic type, in contradis- 
tinction to the paraplegia of spinal disease. The 
paralyzed limbs do not, as a rule, waste, but in time 
they become rigid. 

Paralysis of cranial nerves. 

Paralysis of sensation, mostly either hemianaesthesia or 
affections of special senses. 

Convulsions, particularly if they be limited to a particular 
part of the body. 

Optic neuritis. 
Others, less definite in their meaning, but nevertheless suffi- 
cient to direct our attention to the state of the brain, are — 

Headache. 

Local pain, or tenderness to pressure or percussion. 

Vomiting. 

Coma in its various degrees. 

Delirium. 

Mental affection. 

(2) Symptoms indicative of disease of particular parts of 
the brain : — 

A. Of the cortex cerebri, and of the subjacent white 
250 



ORGANIC CEREBRAL DISEASE. 25 I 

matter. There are two main classes of symptoms — those 
which indicate destruction of nerve-tissue (paralysis), and 
those which indicate its irritation (convulsive movements, 
sensory aurge, etc.). The irritative phenomena are generally 
better marked in cortical than in sub-cortical disease ; the 
paralytic are much the same in both.* 

a. Frontal lobes. No very definite symptoms can be con- 
nected with disease of these parts. We except for the present 
Broca's convolution. 

/?. Motor area {vide pp. 60-63). 

Paralysis of the face, arm, leg, or even of such small parts 
of them as the thumb, hallux, toes, fingers, etc. The paralysis 
is limited — i. e., is a strict " monoplegia" — when the lesion 
is limited and non-progressive. In a progressive lesion the 
paralysis spreads from the face to the arm and leg, or vice 
versa, till the patient becomes hemiplegic. 

Coiwulsio7is . — These also have a local character. They 
begin in a definite part, not unfrequently the thumb or great 
toe, and spread in a definite manner (e.g., from the thumb, 
up the forearm, then down the lower limb, and to the face ; 
or up the lower limb, down the upper, and to the face). Con- 
sciousness may either not be lost at all, or not till the convul- 
sions have spread over a considerable area. Afterwards, the 
parts which have been specially convulsed often exhibit a 
temporary paralysis. The focus of disease is to be sought in 
the cortical centre for the part wherein the convulsions first 
begin. The spread of irritation to adjacent centres is shown 
by the definite way of spreading or " march " of the convul- 
sions. This type of fit, called sometimes " Jacksonian epi- 
lepsy," sometimes " epileptiform convulsion," is of particular 



*That is to say, destruction of a cortical centre produces the same effect 
as destruction of the fibres which connect it with the parts below (pedun- 
cular fibres). Destruction of the fibres connecting centre with centre 
(commissural and associative fibres, vide p. 64) may have different effects. 



252 NERVOUS DISEASES. 

importance, because it indicates local, and probably organic, 
disease. The probability of organic disease is rendered still 
greater if double optic neuritis be present ; we should always 
carefully look for it. 

y. Occipital lobes. 

Hemianopia indicates disease of this part, or of the fibres 
which connect it with the lower visual centres (optic radia- 
tions), or of the optic tract. The half field on the opposite 
side to the lesion is lost. Disease of the angular gyrus perhaps 
causes impairment of vision in the opposite eye. Visual 
spectra may occur in connection with irritation of these parts. 

d. Temporo-sphenoidal lobe. 

At the anterior extremity of this (region of the uncus or 
subiculum cornu Ammonis) is the centre for taste and smell. 
Cases of tumor here are on record wherein fits were present 
beginning with aurse of taste and smell. Quite at the other 
end of the lobe (posterior part of the first convolution) is the 
centre of hearing. Enlargement of the temporo-sphenoidal 
lobe (as in abscess or tumor) may by pressure cause symptoms 
referable to adjacent parts. — e.g., hemianopia from pressure 
on the optic tracts, hemiplegia or hemiplegic convulsions in 
face, arm, leg of the opposite side from pressure on the internal 
capsule or on the motor convolutions. 

If the temporo-sphenoidal lobe, or the island of Reil, of 
the left side be diseased, it is probable that there will be 
aphasia of the sensory type (word-deafness or word-blindness.) 
Aphasia of the motor type (inability to express thoughts in 
words with retention of the capacity for understanding speech 
and writing) is mostly indicative of disease of the posterior 
part of the left third frontal convolution (Broca's convolu- 
tion). 

B. Region of the basic ganglia. 

The capital symptom is hemiplegia of the opposite side 
from interference with the posterior limb of the internal 
capsule, or hemiansesthesia when the posterior extremity of 



ORGANIC CEREBRAL DISEASE. 253 

its posterior limb is affected. Disease in the neighborhood 
of the posterior part of the capsule may also cause choreoid 
movements of the opposite side (Charcot). 

C. Of the cerebellum. 

Disease of the cerebellum (or at least of its middle lobe) is 
indicated by a disturbance of equilibrium leading to an 
unsteady, reeling gait, and finally inability to stand. There 
may be rigidity of the trunk muscles causing retraction of 
the head and opisthotonos. The pressure of a cerebellar 
tumor may cause : (1) an accumulation of fluid in the cerebral 
ventricles, which in young children shows itself by enlarge- 
ment of the head ; (2) paralysis of the limbs from compression 
of the pyramidal tracts ; (3) nystagmus or even oculo-motor 
palsy from compression of the nucleus and root-fibres of the 
third nerve; (4) facial and auditory paralysis from a similar 
cause. Absence of tendon-reactions, an occasional effect of 
intra-cranial disease, is perhaps more frequent in disease of 
the cerebellum than in that of other parts. (The combination 
of absent tendon-reactions with unsteadiness of gait must not 
be mistaken for tabes dorsalis.) 

D. Of the corpora quadrigemina. 

The symptoms (as enumerated by Nothnagel) are not unlike 
those of cerebellar disease — viz., unsteady gait, with which is 
associated nystagmus and ocular paralysis. This latter is 
usually incomplete, the up and down movements of the eye- 
balls being affected more than the other movements. 

E. Of the pons and medulla. 

A lesion sufficiently extensive to affect both lateral halves 
causes paralysis of all four limbs (cervical paraplegia). Such 
a lesion is often a hemorrhage ; contraction of the pupils is 
then apt to occur, presumably from irritation of the adjacent 
oculo-rnotor nuclei or fibres. 

There may be vaso-motor disturbances and hyperpyrexia. 

A lesion of one-half the pons causes cross-paralysis — i. e., 
paralysis of one third, sixth, or facial nerve (according to the 



254 NERVOUS DISEASES. 

level of the lesion), combined with hemiplegia or, it may be, 
hemianaesthesia of the other half of the body. 

Tumors of the pons are characterized by the progressive 
paralysis of cranial nerves and of the limbs. 

An acute lesion of the medulla of any magnitude is incom- 
patible with life ; the commonest chronic affection is pro- 
gressive bulbar paralysis, described as above (p. 236). 

Glycosuria has been observed in tumors of the fourth 
ventricle (in correspondence with the facts ascertained about 
glycosuria produced experimentally). 

Diseases of Cerebral Dura Mater. — Chronic inflam- 
mation of the dura mater may take the form of thickenings of 
the membrane with adhesions to the brain beneath, or that of 
a sub-dural haematoma, which we have already described 
{vide p. 86). In either case the symptoms are so indefinite 
that we shall not describe them here. Acute inflammation of 
the dura occurs chiefly in diseases or injuries of the cranial 
bones (of which indeed it forms the internal periosteum). 
The membrane may simply look dark and discolored, or pus 
may collect between it and the bone. In ear disease, with 
caries of the petrous bone, the condition under which it 
commonly occurs, such an inflammation may be marked by 
no further symptom than exacerbation of the pain in the 
neighborhood of the ear. It would seem, however, that such 
severe symptoms as drowsiness, twitchings, and even optic 
neuritis may develop, which suggest general meningitis or 
cerebral abscess, but that nevertheless recovery may take 
place. 

Tumors may originate in connection with the dura mater; 
they give rise to symptoms in so far as they affect the cerebral 
surface beneath or the outgoing nerve-trunks. 

Thrombosis of Sinuses. —Along with affections of the 
dura mater we may consider thrombosis of the cerebral 
sinuses. This arises either (1) together with inflammation of 
the dura or under the influences of causes that affect the dura 



THROMBOSIS OF SINUSES. 255 

(ear disease, bone disease, injury, etc.) ; or (2) from such 
causes as may produce thrombosis of veins elsewhere — viz., 
the puerperal state, pyaemia, marasmus, sluggishness of circu- 
lation from heart disease, gout (?). The symptoms of intra- 
cranial thrombosis are — pain, oedema of the parts drained by 
the sinus, where these can be observed (thus, in thrombosis of 
the lateral sinus there may be a puffy swelling behind the ear, 
in the district of the emissary vein ; in thrombosis of the 
cavernous sinus oedema of the eyelids), disorders of cerebral 
functions. It is true these characters may be insufficient to 
establish a diagnosis. Thus, in ear disease, where there is 
already pain, and where the mastoid region may be already 
swollen from disease of the cells beneath, and where brain 
symptoms may be present from other causes, it may be 
impossible to tell when the lateral sinus becomes thrombosed. 
A symptom that may help us to diagnose this is the presence 
of tenderness and induration along the course of the internal 
jugular vein (Bowlby), but this is not necessarily present. 

Thrombosis of the longitudinal sinus and of the veins 
emptying into it has been observed to give rise to (1) pain in 
the head ; (2) convulsive twitchings, first in one upper limb, 
then in the other, evidently due to irritation of the cortex 
cerebri; * thrombosis chiefly of the straight sinus and velum 
interpositum to give rise to extreme congestion of both optic 
thalami, and hemorrhagic softening of the right thalamus 
with hemorrhage into the right lateral ventricle ; the symp- 
toms in this particular case being mainly — headache, vomit- 
ing, stupor, twitching of fingers, especially the left hand, with 
some paralysis of the left hand. 

Thrombosis of the cavernous sinus f was indicated by prop- 



*Sir Dyce Duckworth, "Clinical Society's Transactions," vol xxiii; and 
Mr. Arbuthnot Lane, in same volume. 

f Dr. Sidney Coupland, " Ophthalmological Society's Transactions," 
vol. vii, p. 228. 



256 NERVOUS DISEASES. 

tosis of the eyes, pain in the forehead (from irritation of the 
frontal division of the fifth nerve), ophthalmoplegia from 
involvement of the motor nerves of the eye in their passage 
through the walls of the sinus ; there was in this case no 
oedema of the lids. 

Acute General Meningitis of Cerebral Pia Mater. 
— In a well-marked case of acute general meningitis, puriform 
lymph is found covering the surface of the brain, on the con- 
vexity as much as the base, held in the meshes of the sub- 
arachnoid space. It may form an almost uniform layer, or 
may be principally distributed along the course of the vessels. 
The brain itself may be injected and softened. The choroid 
plexus may share in the inflammation of the meninges, and 
then there is turbid fluid in the ventricles, and the ganglia 
may be softened. We have already enumerated the causes of 
such a disease {vide p. 87). 

Fever and pain in the head are early and constant symp- 
toms. The height of the temperature may vary much in 
different cases. The headache is very severe, and by no 
means proportionate to the fever. There will probably be 
signs of so-called cerebral irritation — e.g., injection of the 
conjunctivae, photophobia, sensitiveness to noise, dislike of 
being touched or disturbed. Vomiting may be expected, 
and that apart from food. Examination of the fundus oculi 
may show the presence of optic neuritis ; if so, we may con- 
clude that the foregoing symptoms are due to actual intra- 
cranial disease; but if there be no neuritis, we cannot draw 
the opposite conclusion. But sometimes convulsions, or 
partial paralysis, especially paralysis of the ocular muscles, 
may occur to stamp the disease as cerebral. The head is often 
drawn back, the muscles at the back of the neck being rigid ; 
this is thought to indicate meningitis at the base of the brain, 
or of the upper cervical cord. Retraction of the abdominal 
wall may sometimes be seen. On the side of the vascular 
system there may occur (1) the tache cerebrale — that is to say, 



TUBERCULAR MENINGITIS. 257 

the ready appearance of a white streak, bordered by red flush, 
when the finger-nail has been drawn across the skin ; (2) 
abnormalities in the pulse-rate, which, instead of mounting 
pari passu with the temperature, may remain infrequent, while 
the rhythm of the pulse is somewhat irregular. 

As the disease advances, the pain and symptoms of irritation 
give place to an apathetic condition, which deepens into 
coma. This may or may not be accompanied by actual 
paralysis. The pulse-rate quickens, the respiration becomes 
embarrassed, and the temperature may rise very high. Some- 
times meningitis (especially in those instances where it com- 
plicates grave pre-existing disease) manifests itself only by 
the sudden access of fatal coma. 

Undoubtedly, some patients recover from even grave symp- 
toms of meningitis, but the severe attacks, as a rule, prove 
fatal. Patients with chronic ear disease are sometimes seized 
with severe pain in the head, fever, and perhaps even optic 
neuritis, which all prove transient. It is conceivable in such 
a case that the inflammation has not advanced beyond the 
dura (p. 254). The remedies usually applied are applica- 
tion of cold to the shaven head, leeches to the mastoid region 
(or even general blood-letting), a smart mercurial purge, 
saline draughts or iodide of potassium ; and for the head- 
ache, bromide or morphia, if necessary. 

Tubercular Meningitis. — By far the commonest form 
of meningitis is that due to tubercle. Its morbid anatomy 
we have already described. Its symptoms are essentially the 
same as those of a simple meningitis, but may manifest them- 
selves in a somewhat different fashion. They develop more 
gradually, and are on the whole less severe, though the event 
appears to be uniformly fatal. The patient is usually *a child 
from three to twelve years of age. The health may have been 



* Vide table of eleven cases in adults, in Dr. Norman Moore's " Medical 
Pathology," p. 161. 



258 NERVOUS DISEASES. 

failing for some time previous to the outbreak of the disease ; 
there has been change of disposition, sleeplessness, cough, 
and wasting and the like. Then fever develops, usually not 
of high degree, headache, vomiting, perhaps convulsions. 
The diagnosis will have to be made from a febricula in a 
nervously disposed subject, or from typhoid fever. The 
abdomen is retracted, not distended nor tender, as in typhoid ; 
there is no rash, the temperature does not mount regularly, the 
pulse is apt to be infrequent and slightly irregular. The tendon- 
reactions are said to be normal, diminished, or absent,* not 
increased, as in typhoid. Sometimes optic neuritis is to be 
found. Sometimes also tubercles may be seen upon the 
choroid. While asleep the child often utters a short sharp 
cry, known as the "hydrocephalic cry." The head is re- 
tracted. Paralysis of the cranial nerves, when it occurs, is 
important as indicating probable mischief at the base of the 
brain, the part upon which tubercular meningitis specially 
concentrates itself. But hemiplegia may appear, or unilateral 
convulsions of one limb and that without a correspondingly 
localized lesion to be found post-mortem, for the functional 
disturbance extends far beyond the area of the brain actually 
affected with tubercle. Before the second and fatal stage of 
coma sets in, there may be a temporary improvement in all 
the symptoms, likely to inspire misleading hopes of recovery. 
We have stated that tubercular meningitis is almost always 
associated with tubercle elsewhere, is often, indeed, part of a 
general tuberculosis. On this account, in a doubtful case of 
cerebral disease, the presence of strumous glands, phthisis in 
the lungs, or even a strong family history of phthisis, makes 
it all the more probable that the disease is tubercular menin- 
gitis. The fact may also help to explain the great fatality of 
the disease. 

* This may be due in some cases to the presence of spinal meningitis, in 
others absence of knee-jerk is seen where the lesion is purely cerebral. 



EPIDEMIC CEREBRO-SPINAL MENINGITIS. 259 

Basal Meningitis or Cervical Opisthotonos of In- 
fants. — Under the head of " cervical opisthotonos of in- 
fants," Drs. Gee and Barlow* have described a form of 
meningitis affecting the base of the brain, particularly the 
neighborhood of the occipital foramen, and gluing together 
the cerebellum and medulla. The causation of it is not fully 
determined. It affects children under two years of age, and 
therefore occurs earlier in life than tubercular meningitis is 
wont to do. The essential symptom of it is holding back of 
the head (which in other forms of meningitis is common but 
not essential). The onset may be sudden or gradual ; some 
children recover soon, some die, in others the disease persists 
for many months. In addition to the retraction of the head, 
there may be fever and vomiting, rigidity of limbs, convul- 
sions, and hydrocephalus. This last symptom is presumably 
due to closure of the communication between the spinal canal 
and cerebral ventricles. 

Epidemic Cerebro-spinal Meningitis. — Epidemic 
cerebro-spinal meningitis is an acute specific disease, wherein 
the effects of the poison manifest themselves chiefly by inflam- 
mation of the meninges, just as diphtheria localizes itself upon 
the fauces, and typhoid upon Peyer's patches. It is uncom- 
mon in this country. Its origin can generally be traced to 
defective sanitation. In addition to fever, pain in the back, 
and other symptoms of acute meningitis, cerebral and spinal 
(which we need not repeat again), there is often severe 
abdominal pain, and a petechial eruption occurs (from the 
second to the fourth day). Death may occur from collapse, 
even before the meningitis has manifested itself. Sporadic 
cases of this disease are sometimes seen, and this possibility 
should be borne in mind when a case of acute meningitis 
presents itself, for which no cause can be found. 

Syphilitic meningitis is less acute and more localized than 

* "St. Bartholomew's Hospital Reports," vol. xiv, p. 23. 



260 NERVOUS DISEASES. 

the forms we have described. We shall reserve the consider- 
ation of it for the present. 

Cerebral Abscess. — Inflammation of the brain substance 
takes place in cases of meningitis, and also in the neighbor- 
hood of tumors, hemorrhages, and the like. It is likely that 
encephalitis may also arise as a primary disease, but as yet we 
know little of it, save of that localized form of it which ter- 
minates in abscess. The diagnosis of cerebral abscess is often 
a matter of much difficulty ; it may, indeed, be impossible, and 
that for the following reasons, (i) A chronic abscess may ex- 
ist for long without giving rise to any symptoms. (2) Symp- 
toms when they do arise are not necessarily distinctive of ab- 
scess, as contrasted with other diseases of the brain or of its 
membranes. This is true both of the general symptoms and 
of the localizing symptoms. The former may indicate in a 
vague way grave cerebral disease, the latter disease of a par- 
ticular part of the brain, without giving us a clue as to what 
the nature of that disease is. (3) The conditions which lead 
up to the development of cerebral abscess, notably ear-dis- 
ease with caries of the petrous bone, may themselves give rise 
to cerebral symptoms — e.g., headache, vomiting, vertigo, fever 
— without the actual formation of abscess. 

The possibility of an abscess must not be forgotten in any 
case of obscure cerebral disease ; but that possibility presents 
itself most forcibly when one of the recognized causes of cer- 
ebral abscess actually exist. These causes (to recapitulate 
them from p. 76), are chronic disease of the middle ear or of 
the nasal cavities, disease of the cranial bones, injury to the 
head, pyaemia, empyema, bronchiectasis. By far the most 
frequent cause is chronic ear-disease, and we shall therefore 
address ourselves to this condition. Where grave cerebral 
symptoms arise in the course of a chronic otitis, which treat- 
ment of the ear-disease- fails to relieve, an abscess may be sus- 
pected, particularly if the localizing symptoms point to the 
sites which such abscesses specially choose — viz., the temporo- 



CEREBRAL ABSCESS. 26 1 

sphenoidal lobe or the cerebellum. And if we can exclude 
such other sequelae of chronic otitis as meningitis, disease of 
the lateral sinus, pyaemia,* the diagnosis of abscess may be 
considered probable. 

We will consider briefly, (1) the otitis itself; (2) the gen- 
eral cerebral symptoms indicative of abscess ; (3) the symp- 
toms (if any) indicative of its locality. 

(1) The otitis is usually chronic, and accompanied by dis- 
ease of the mastoid cells or caries of other parts of the 
petrous bone. (Facial paralysis of the peripheral type and 
on the side of the affected ear may be an indication of such 
caries.) The cerebral symptoms may follow an exacerbation 
of ear trouble such as acute pain in the ear, suppression or 
great increase of discharge, etc ; but such a sequence is by no 
means necessary. For an abscess, formed long ago, may 
have remained "latent" till some cause quite independent of 
the original ear-disease lights up mischief around it and so 
gives rise to symptoms. The otitis itself, or some complica- 
tion short of abscess (possibly inflammation of the dura mater?), 
may give rise to serious cerebral symptoms, as we have already 
said ; it would appear that even optic neuritis may arise in 
this way. This fact complicates the diagnosis ; but the prac- 
tical lesson is that the ear-disease, mastoid disease, etc., 
should be promptly treated and the effect of such treatment 
closely watched. 

(2) The general symptoms. These, as we have said, are 
not necessarily distinctive. The commonest are — pain in the 
head, possibly at the seat of the abscess ; perhaps local tender- 
ness also; drowsiness, stupor, coma, sometimes delirium; 
optic neuritis, paralysis. The temperature often remains low. 
Convulsions, violent delirium, and acute symptoms generally 



* It must be remembered, however, that any one of these three may 
co-exist with abscess; and further, that to exclude them definitely may 
be almost impossible; we can only proceed on probabilities. 



262 NERVOUS DISEASES. 

point rather in the direction of meningitis than of abscess, 
though no absolute rule can be laid down. 

(3) The localizing symptoms. These may be very im- 
perfect : there may, indeed, be none. An absence of the 
temporo-sphenoidal lobe might be expected to induce some 
abnormality of taste, smell, or hearing ; but the patient is 
generally deaf from other causes, and may be in too dull a 
state for testing of the senses. The same reason may obscure 
such symptoms as hemianopia and aphasia, though these have 
been made out. Hemiplegia of the opposite side, involving 
successively face, arm, and leg, may occur ; this being the order 
of proximity of the motor centres and their peduncular fibres 
to the temporo-sphenoidal lobe. Ptosis and inequality of 
pupils may be seen. But the site of the abscess is more 
often guessed from our knowledge that this lobe is the com- 
monest site, than deduced from the actual symptoms. 

The only means of cure for an abscess is to open and drain 
it. This has been done successfully in several instances; and 
since the disease when once serious symptoms have arisen 
is certain to end fatally, it seems reasonable to trephine and 
open the abscess, when once we are convinced of its presence 
and locality. But if, as is more often the case, we only 
strongly suspect it, the only course is first to treat the ear 
disease thoroughly, and then, if the patient still remain in a 
critical condition, trephine and puncture the temporo- 
sphenoidal lobe. A successful issue, even if pus be evacuated, 
must not be too confidently expected ; for it is always possible 
that the abscess may have ruptured into the ventricles or into 
the meninges before the treatment has been undertaken. 

Abscess of the cerebellum may be suspected in a case of 
otitis, where there is occipital headache, vertigo, and stagger- 
ing gait. But it may give rise to no localizing symptoms. 

Abscess in other parts can only be diagnosed when there 
are localizing symptoms pointing to disease at a definite part 
of the brain, and when there is present some one of the known 



CEREBRAL HEMORRHAGE. 263 

causes of intra-cranial abscess. It is evident that an abscess 
near the cortex of the motor area may be dealt with surgically, 
provided we can localize it accurately, and provided that it 
has not extended too deeply. 

Cerebral Hemorrhage. — Cerebral hemorrhage occurs 
most commonly in connection with atheroma of the cerebral 
arteries, and more particularly when such arteries are subjected 
to a high arterial pressure, as is the case in chronic Bright' s 
disease. In a large proportion of the patients brought in dead 
into hospital we find the following associated facts : cerebral 
hemorrhage, atheroma of cerebral vessels, hypertrophied left 
ventricle, granular kidneys, gout. According to some authori- 
ties, hemorrhage does not take place until small aneurisms 
have formed ; the rupture of one of these determines the 
hemorrhage. These are called miliary aneurisms ; they are 
numerous and very small, amd are to be seen, after macerat- 
ing away the brain substance and clot, studded along the 
vessels. Or the blood may come from numerous capillary 
vessels. Cerebral hemorrhage most frequently originates, as 
we have already said, from a branch of the middle cerebral 
artery which skirts the outer side of the lenticular nucleus. 
Aneurisms of a larger kind, generally about the size of a pea, 
may rupture and give rise to hemorrhage ; these may be 
seated on the larger trunks (meningeal or circle of Willis) ; 
their origin may sometimes be traced to previous embolism. 
Fatty degeneration of arteries, vascular tumors, venous nsevi, 
the congestion consequent on venous thrombosis, etc., are 
other, though rare, causes of cerebral hemorrhage. We omit 
here the intra-cranial hemorrhages caused by fracture of the 
skull and laceration of the brain from injury. 

The usual sites for hemorrhage may perhaps be given in 
this order : neighborhood of the basic ganglia (as above de- 
scribed), pons, meninges, centrum ovale and convolutions, 
cerebellum, these last-mentioned sites being uncommon. 

Let us consider the commonest forms of cerebral hemor- 



264 NERVOUS DISEASES. 

rhage. The patient is usually of middle age or past it, since 
the liability to arterial disease and granular kidney increases 
with advancing years. He may have been in good health till 
the actual attack, or at most may have had such slight "warn- 
ings" as headache, giddiness, or even transient attacks of loss 
of power, numbness, and pargesthesise. The leading features 
of the attack are coma and hemiplegia, but their mode of 
onset may vary. In a small hemorrhage there may be no real 
coma ; the patient may be merely faint, giddy or sick, or 
even lose the use of his limbs without any such accompany- 
ing affection. Or he may wake from his night's sleep and 
find himself paralyzed ; or he may experience some strange 
sensation of numbness, tingling, etc., in the limbs about to 
suffer, and perhaps lose power in them, and then will come 
the loss of consciousness. Cases where the symptoms of 
paralysis and coma come on by degrees, but advance steadily 
hour by hour, have been called " ingravescent apoplexy," and 
are said to be always fraught with danger. Lastly, the patient 
may be stricken down suddenly, unconscious and paralyzed, 
an apoplexy in the original and etymological sense of the 
word. However it has arisen, in a cerebral hemorrhage of 
any severity we usually find the patient comatose. The depth 
of this coma, as indicated by the impossibility of rousing him, 
the stertorous breathing, laboring pulse, relaxation of the 
limbs, difficulty of swallowing, blunting of reflex action, and 
the persistence of the coma, are a measure of the gravity of 
the case. He may die in this condition, or he may not 
recover consciousness for several days. The hemiplegia may 
be somewhat masked while the patient is deeply unconscious. 
We have already mentioned the points to look to {vide p. 97) 
— viz., whether the limbs of one side fall, when raised, in a 
more flaccid and inert way than those of the other, whether 
the face is drawn (we need hardly add the distortion is toward 
the non-paralyzed side), whether one cheek is more puffed out 
than the other. Further, we should note whether the eyes 



CEREBRAL HEMORRHAGE. 265 

and head turn to one side, remembering (1) that the presence 
of such a "conjugate deviation" is reckoned a symptom of 
some gravity. (2) That the deviation of the head and eyes, 
in a paralyzing lesion of one hemisphere, is toward the side 
of the lesion. The state of the tendon-reactions at this stage 
will probably be of little help toward diagnosing the hemi- 
plegia. As regards the skin-reflexes, it has been asserted that 
in the early stages of a hemiplegia they are absent on the 
paralyzed side, though retained on the other side. 

In some cases there are convulsions. Their presence leads 
us to suspect that the hemorrhage involves the meninges or 
has ruptured into the ventricles ; should either event have 
happened the prognosis is bad. It is quite possible, however, 
that convulsions may occur merely as the effect of irritation, 
and it should be remembered that in some severe epileptic 
attacks there is transitory hemiplegia — a combination which 
may simulate hemorrhage with convulsions. Sometimes the 
paralyzed limbs are rigid, even at this early stage ; this prob- 
ably is also caused by the irritation of the hemorrhage. The 
bladder is likely to become distended, and therefore the hypo- 
gastrium should always be examined and the urine drawn off 
if necessary. 

The first danger, immediately after the attack, is collapse 
from the shock of the hemorrhage. If the skin be cold, the 
body temperature low, and the pulse feeble, small doses of 
brandy or diffusible stimulants must be given, and warmth 
supplied to the epigastrium and the limbs. The second is 
probably from gradual increase of the hemorrhage, indicated 
by increasing coma and paralysis spreading to the organic 
reflexes of swallowing, respiration, etc. A large or advancing 
hemorrhage will probably rupture into the cerebral ventricles; 
this is a fatal complication. Whether any medical means can 
arrest hemorrhage is somewhat questionable ; it is, at any rate, 
advisable to keep the patient at absolute rest, with the head 
slightly raised, and cool ; usually a purge, calomel or croton 



266 NERVOUS DISEASES. 

oil. is given, and mustard plasters applied to the calves. A 
third danger appears later, during what we may consider the 
period of reaction, from a day or two to a week after the 
attack. After some initial improvement, perhaps after con- 
sciousness has begun to return, the temperature rises and 
continues to mount steadily, then the respiration becomes 
embarrassed, the face becomes blue, and the skin clammy ; 
finally, the patient dies, apparently from the side of the 
lungs. After death in this way there is found extreme 
engorgement of these organs; and since the lung on the 
paralyzed side suffers most, it has been urged that such 
" congestive pneumonia " is really a trophic lesion depending 
directly on the paralysis. The same remark applies to another 
phenomenon sometimes seen at this stage — viz. , the appearance 
of an acute bedsore on the buttock of the paralyzed side. 

In more favorable cases consciousness returns ; the amount 
of the hemiplegia will now be more easy to estimate. We 
next begin to look for improvement of the hemiplegia; and 
however complete the paralysis be at first, it does not follow 
that it may not improve — perhaps in a few days, perhaps in a 
few weeks. 

The earlier such improvement begins, the quicker it goes 
on. Sensory paralysis, if there be such, usually mends sooner 
than the motor ; the movements of the leg return before those 
of the upper limb, and those of the arm and forearm before 
those of the thumb and fingers. But there may be little or 
imperfect amendment, and the patient then remains a chronic 
hemiplegic. 

Varieties According to Site of Lesion.— Hemorrhage 
into the pons is necessarily graver than hemorrhage into one 
hemisphere; it is distinguished by the contracted state of the 
pupils, and by the fact (if the distribution of the paralysis can 
be made out) that either all four limbs are paralyzed or that 
there is cross-paralysis. Vaso-motor disturbances and high 
rises of temperature are apt to take place. 



CEREBRAL HEMORRHAGE. 267 

Meningeal hemorrhage is almost always fatal ; convulsions 
or twitchings of the limbs and delirium are common accom- 
paniments. Thus it is liable (as Dr. Wilks remarks) to be 
taken for ursemia. 

We need hardly add, that according to the amount of the 
hemorrhage so the symptoms may vary in degree from those 
of a fatal disease to such as scarcely interrupt the patient's 
avocations ; and according to the position of the hemorrhage, 
so may the paralytic symptoms vary in kind. The ordinary 
form of paralysis, hemiplegia, is caused by pressure on or 
rupture of the internal capsule. Where there has been mere 
pressure the paralysis may recover ; where the capsule has 
been destroyed, it remains lastingly. 

Cerebral Softening from Arterial Obstruction. — 
Softening of the brain substance, apart from that produced by 
venous congestion (which we have alluded to under the head 
of thrombosis of the sinuses) and apart from that produced 
by inflammation in the neighborhood of a tumor or a menin- 
gitis, is produced by obstruction of the cerebral arteries. 
The central cerebral arteries are terminal, and those of the 
meninges have not free anastomoses; hence the block of any 
vessel beyond the circle of Willis produces immediate loss of 
blood-supply, and therewith loss of function, and next a 
necrosis of the brain tissue, which manifests itself post-mortem 
as softening, in the district of the blocked artery. 

Embolism and Thrombosis. — The arterial block may 
be due either to embolism or thrombosis. Emboli generally 
consist of fragments swept by the circulation from a diseased 
cardiac valve; or it may be of portions of clot from the 
interior of an aneurism; their favorite place of lodgment is 
the middle cerebral artery at one or other of its bifurcations, 
and more often, it is said, the left middle cerebral than the 
right. Thrombosis may take place in any artery ; the two 
main causes thereof are syphilitic arterial disease (which we 
shall discuss later on) and atheroma. 



268 NERVOUS DISEASES. 

Between the symptoms of cerebral softening and those of 
cerebral hemorrhage no distinction can be drawn that is ab- 
solutely diagnostic. Coma, it is said, more frequently ac- 
companies the latter ; but as in a slight hemorrhage coma may 
be absent, so it may be present in an extensive and sudden 
softening. Perhaps in a hemorrhage of any degree the 
phenomena of shock are likely to be more severe than in 
softening. Softening from embolism would seem to entail a 
very sudden onset of paralysis, whereas in hemorrhage there 
may be prodromata ; but in softening from thrombosis the 
paralysis may develop (though this is not invariable) by 
degrees. In some few instances, embolism of the arteria cen- 
tralis retinae may be seen, and may be taken as the index of 
an analogous process within the brain. Sounder distinc- 
tions are perhaps to be sought in the antecedents and consti- 
tution of the patient. When he is of middle age or past, and 
has a hard pulse with tortuous temporal arteries, a heaving 
cardiac impulse, and watery urine containing a trace of albu- 
men, with, may be, a gouty history, we suspect a hemorrhage. 
In old people with calcareous arteries and feeble circula- 
tion, we think of thrombosis from atheroma. Thrombosis 
in younger people is mainly the result of syphilitic arteritis. 
In a young patient with signs of valvular disease, hemiplegia 
is most reasonably explained by embolism. Yet we have 
twice seen, recently, the following order of events: a pa- 
tient, who is in hospital for severe heart disease, becomes 
suddenly unconscious and hemiplegic; embolism is naturally 
diagnosed ; but post-mortem hemorrhage is found from an 
aneurism, the aneurism having probably been caused by some 
previous embolism. Though speedy death may unques- 
tionably result from extensive softening, hemorrhage is the 
most dangerous process to life ; on the other hand, the prog- 
nosis, quoad recovery, is worst in softening ; for here the 
paralysis depends mainly on destruction of tissue, whereas in 
hemorrhage it may be largely due to the effects of pressure. 



LATE HEMIPLEGIA. 269 

The Characters of Confirmed Hemiplegia. — Perma- 
nent hemiplegia is produced by destruction of the motor tract 
in the internal capsule, or indeed above that level, provided 
the lesion be sufficiently extensive ; and the hemiplegia has 
eventually the same characters, whatever was originally the 
nature of the lesion. It is worth while considering this con- 
dition of "late hemiplegia." The distribution of motor 
paralysis, the presence or absence of aphasia and of sensory 
abnormalities, is mainly dependent on the seat of the original 
lesion. Commonly, however, sensory paralysis, and to a 
certain extent speech difficulties,* tend to disappear, and the 
paralysis of the leg and face mend sooner than that of the 
upper limb, and the coarse movements at the shoulder and 
elbow return sooner than the fine movements of the fingers 
and head. A striking feature of a permanent hemiplegia is 
rigidity. Such rigidity, when developed slowly at some dis- 
tance of time from the original attack, is due to a descending 
degeneration of the pyramidal tract. Its advent is heralded, 
as a rule, by the appearance of exaggerated tendon-reactions 
and ankle-clonus in the paralyzed limbs. We have already 
described the position which the rigid limbs assume — the stiff, 
extended leg, the clenched fingers, the semi-flexed and semi- 
pronated forearm {vide p. 112). Occasionally the tendon- 
reactions become exaggerated on the sound side as well, and 
in rare cases there may be double ankle-clonus, with even rigid- 
ity and paralysis of both legs. This seems to indicate some 
spread of the degeneration to the pyramidal tract of the 
sound side ; we do not precisely know the mechanism of it. 
Another rare complication is the appearance of muscular wast- 
ing with electrical changes due to the advance of degeneration 



* This probably does not bold good for aphasia dependent on cortical 
or sub-cortical disease; but the minor forms of speech difficulty, mostly 
difficulties of articulation, which accompany right hemiplegia, generally 
improve before the hemiplegia itself. 

2 3 



27O NERVOUS DISEASES. 

from the pyramidal tracts to the anterior cornual cells. In- 
voluntary movements form another class of complications. 
Most commonly such movements are of the kind known as 
athetosis (vide p. 102) — viz., slow continuous movements, prin- 
cipally of the fingers, hand, and forearm ; these are seen mostly 
when the hemiplegia is incomplete and when it has originated 
in early life. Less often there is ataxia of the paralyzed limbs 
or tremors, suggestive of disseminated sclerosis or even of 
paralysis agitans. Pain in the paralyzed limbs is not infre- 
quent ; it appears to arise spontaneously, may be very severe, 
and is refractory to treatment. Convulsions are frequently 
associated with hemiplegia. The association may be of vari- 
ous kinds : thus, in children, hemiplegia may follow immedi- 
ately upon an attack of convulsions ; the hemiplegia persists 
and the convulsions are repeated at intervals; probably both 
symptoms are due to some one common cause. Similarly, in 
adults, an arrested cortical lesion (generally a gumma or a local 
meningitis) may give rise both to hemiplegia and to convul- 
sions. But there is a variety of convulsion which may be 
more truly called " post-hemiplegic." Here the hemiplegia 
originates in some ordinary vascular lesion, hemorrhage, em- 
bolism, or the like ; after a time, and without apparent spread 
of the disease, a fit of convulsions takes place, and subse- 
quently others. Sometimes their connection with the hemi- 
plegia is shown by the fact that they are limited to or com- 
mence in the paralyzed limbs ; sometimes they are general 
convulsions with loss of consciousness, and recurring with 
tolerable regularity, like true epileptic fits, and remediable, 
like them, by treatment with bromide. In most cases of hem- 
iplegia the mental functions are not affected ; but occasionally 
the patient becomes gradually irritable, forgetful, or foolish. 
Where the hemiplegia is dependent on such arterial disease as 
atheroma or syphilis, such symptoms may be reasonably 
ascribed to general cerebral mal-nutrition. 

Double Hemiplegia, or " Di-plegia." — It may hap- 



HEMIPLEGIA IN CHILDREN. 2J\ 

pen that a patient has had two attacks of hemiplegia, one on 
each side, and that the effects of both persist. This is called 
double hemiplegia, or di-plegia. In this case functions may 
suffer which escape in ordinary hemiplegia, as, for instance, 
that of swallowing, and perhaps that of micturition. In some 
rare cases the lower face and tongue have been paralyzed from 
a double lesion, one in each cerebral hemisphere. Such a 
condition closely resembles paralysis of the tongue and face 
from disease of their bulbar nuclei (vide p. 235), and has 
hence been called " pseudo-bulbar paralysis." But there is no 
wasting of the tongue, nor change in the electrical reactions. 
Hemiplegia in Children. — Hemiplegia of cerebral ori- 
gin occurs in young children with much greater frequency 
than might have been anticipated. It is distinguished from 
the effects of anterior cornual myelitis (infantile spinal paral- 
ysis ) as follows : (a) by the distribution of the paralysis. 
In the spinal disease a hemiplegic distribution is unusual, and 
the face is never affected. (/?) By the tendon reactions ; these 
are exaggerated in the cerebral disease, normal or absent in 
the spinal.* (/) By the nutrition of the limbs. Although in 
the cerebral paralysis there may be a general shrinking, and 
even shortening, from arrested development of the bones, yet 
the wasting does not, as in the spinal paralysis, pick out groups 
of muscles, and there is no electrical reaction of degeneration. 
The causes of hemiplegia in children are somewhat obscure. 
Doubtless it is sometimes due to embolism or arterial throm- 
bosis (for such thrombosis hereditary syphilis may be respon- 
sible, which is capable, like the acquired disease, of producing 
cerebral arteritis). Other cases may be due to mal-develop- 
ment of the brain or to injury during birth. Infantile 
hemiplegia often sets in with convulsions, as if the seat of the 



* Absent, where the muscle which normally enters into the reaction is 
paralyzed : thus, in atrophy of the quadriceps cruris the knee-jerk is 
abolished. 



272 NERVOUS DISEASES. 

disease were in the cortex. To account for this, two theories 
have been proposed : (1) that the original disease is a throm- 
bosis of the meningeal veins which drain the cortex (Gowers) ; 
(2) that as in infantile spinal paralysis there is an inflamma- 
tion limited to the anterior cornua of the cord, so in the 
cerebral disease there is inflammation of the large cells of the 
motor area of the cortex, acute polio-encephalitis (Striimpell). 

Treatment. — When hemiplegia has persisted for any 
length of time (say for a year), and when, in addition, con- 
tractures of the paralyzed limbs have slowly and steadily 
supervened, we may assume that there is tolerably complete 
descending sclerosis of the pyramidal tract of the paralyzed 
side. Such a condition must be regarded as incurable. It 
may be advisable, with a view of preventing the extreme 
flexion of the fingers, to apply faradism to the extensor 
muscles from time to time, and to practice passive manip- 
ulations of the joints, in order to obviate secondary ankyloses 
and deformities. In milder cases, where there is less contrac- 
ture and some retention of power, faradism may be useful as 
a sort of gymnastic to the muscles. But it must be used care- 
fully, as strong currents are likely to increase contractures. 
Massage is also useful in such cases. The rigidity of lateral 
sclerosis, just like the pains of posterior sclerosis, are aggra- 
vated by cold, hence the limbs should be kept warm, and 
hence an equable climate, free from damp, cold, and from 
biting east winds, is the best for such patients. Hydropathic 
treatment may also be of use. But it is evident that we can 
neither repair the lost nerve-tissue nor obviate the sclerosis 
which follows its loss. 

Cerebral Tumors. — In a case of intra-cranial tumor it 
is obvious that the nature of the tumor will cause differences 
in the symptoms, according to the rate of its growth and the 
degree in which it actually destroys or merely displaces the 
cerebral tissue. Thus, a fibroma which springs from the dura, 
and simply displaces the adjacent brain-substance, may cause 



CEREBRAL TUMORS. 2/3 

next to no symptoms. Malignant tumors, whose advance is 
rapid and unaffected by treatment, cause marked symptoms 
both of nervous irritation and paralysis. In a third class of 
tumors, those due to tubercle or syphilis, we may witness 
sometimes the development of grave symptoms followed by 
their subsequent arrest, it may be as a consequence of treat- 
ment or it may be spontaneously. The nature of an intra- 
cranial tumor, hidden as it is from sight and touch, must be a 
matter of conjecture only, a conjecture based upon the inten- 
sity and rapidity with which the symptoms develop, upon the 
physical condition and history of the patient, and possibly 
upon the occurrence of tumors in other parts of the body. 

General Symptoms. — Of the general symptoms of such 
a disease — i. e., those which indicate its presence without indi- 
cating its locality — the most important are : — 

(i) Pain in the head.. In any rapidly advancing growth 
this is likely to be very severe ; more so than in any other 
form of cerebral disease, excepting perhaps meningitis. It is 
less intermittent than headache from migraine. In any case 
of severe and persistent headache we should examine for the 
next symptom — viz. : — 

(2) Optic neuritis. This, as we have seen, is a sign that 
very frequently accompanies gross organic disease within the 
cranium, and of such organic diseases intra-cranial tumor is 
the one that most frequently gives rise to it. It is present in 
most cases of tumor at some stage or other of their develop- 
ment. In the course of some tumors optic neuritis may be 
observed to appear and to pass on into optic atrophy, the 
tumor all the time continuing its development. Or such a 
"post-neuritic" atrophy may be seen when the patient first 
comes under observation, indicating that a tumor has formerly 
existed, or exists in a quiescent state, or has been developing 
during a considerable time. The exact relation of optic 
neuritis to tumor is not definitely known : we cannot infer 
from the neuritis the position, nor the stage, nor the character 



274 NERVOUS DISEASES. 

of the tumor ; we only know that the two things frequently 
co-exist. 

(3) Vomiting may accompany cerebral tumor. It has been 
ingeniously suggested by Dr. Buzzard that such vomiting 
may be due to a neuritis of the pneumogastric, analogous to 
optic neuritis. We cannot distinguish it from vomiting due 
to cerebral disease of other kinds. From the vomiting of 
gastric disease it is distinguished by the absence of other signs 
of gastric disease, and by the fact that it has no constant rela- 
tion to the ingestion of food ; from the vomiting of migraine, 
by the fact that the headache and other symptoms are not 
terminated by it. 

(4) Coma occurs in the later stages of many cerebral 
tumors. It is doubtless often an index of increased intra- 
cranial pressure, either from mere size of the growth, or from 
the accumulation of intra-ventricular fluid which its pressure 
has occasioned. 

All the symptoms we have enumerated, and in addition 
convulsions, perhaps even localized convulsions, may occur in 
uraemia. Probably they will then appear somewhat brusquely ; 
whereas in organic cerebral disease they have a steady devel- 
opment ; but in any case the urine should be examined, to 
eliminate, if possible, the presence of Bright's disease. 

Localizing Symptoms. — Localizing symptoms, those 
which point to the seat of a tumor, may be absent, vague, 
or precise, according to its position. They attain their 
greatest precision when it is seated in the motor area of the 
cortex. The comparatively slow evolution of a tumor, and 
the fact that it infiltrates the nerve-elements before destroying 
them, usually allows a period of irritation. This is evidenced 
(in the motor cortex) by attacks of convulsions, of the type 
known as epileptiform fits, or "Jacksonian epilepsy." We 
have already described these * as being particularly charac- 

* Vide p. 250. 



CEREBRAL TUMORS. 275 

teristic of organic disease of the motor cortex (more often 
than not a tumor of this part) ; let us emphasize again the 
importance of observing in what member the convulsion 
begins ; because the focus of disease probably corresponds 
with the motor centre for this member ; and the manner in 
which the convulsion spreads ("march of the spasm"), be- 
cause the limbs are often involved in an order which corre- 
sponds to the order of proximity of other centres to the focus. 
The "discharge," as it is called, begins at the focus of dis- 
ease, and the neighboring centres are "let off" in turn. 
The temporary paralysis which often follows in the limbs that 
have been convulsed is reasonably attributed to the exhaustion 
of the centres. But as the disease proceeds this temporary 
paralysis becomes permanent and independent of the con- 
vulsions ; this may be taken to indicate a second stage, in 
which actual destruction of nerve-elements is taking place. 
This stage is important, because the probabilities of complete 
repair are now small, and because it sufficiently distinguishes 
the case from certain puzzling instances in which Jacksonian 
epilepsy occurs without organic disease. If the tumor still 
progresses, it is probable that more general cerebral symptoms 
will arise, such as coma, paralysis of all the limbs, rise of tem- 
perature with pulmonary congestion ; these are usually the 
beginning of the end. If the tumor be arrested, as may be 
seen in cases of gummata principally, the patient's life may 
be saved, but he may remain either non-paralyzed but liable 
to convulsions, or subject to convulsions and withal perma- 
nently paralyzed. This will depend on the amount of damage 
done to the cortex. 

Convulsions which have commenced in the manner just 
described may become, as a case proceeds, so far general that 
it is impossible to be sure of their local origin ; and some- 
times convulsions, which from the outset have been general, 
in association with double optic neuritis may be the only 
indication of a cerebral tumor. 



276 NERVOUS DISEASES. 

Similar symptoms of irritation and paralysis of the sensory 
organs may arise when a growth is situated in the sensory 
sphere of the brain. The difficulty of investigating them is 
much greater than in the case of the motor phenomena, 
neither can we at present refer them with equal accuracy to 
definite parts of the brain. We may notice here that even 
when the tumor is in the motor area, a certain numbness or 
paresthesia may be present in the limbs that are affected by 
convulsions. 

We shall not attempt to describe the symptoms produced 
by growths in each and every part of the brain. We have 
given above {vide p. 251 et seq.~) a short sketch of such local- 
izing symptoms, which will hold good for tumors as well as 
for other diseases. Given a certain set of symptoms, we 
have to think whether they can be explained on the supposi- 
tion that some definite spot in the brain is diseased. Only 
let us remember also the following facts : First, that the 
effects of a tumor may extend far beyond its actual site; obvi- 
ously this holds for effects of irritation, but it holds also for 
paralyzing effects. For softening of brain-tissue may take 
place around the growth, or its pressure may annul the functions 
of nerve-elements that are structurally healthy. Secondly, 
that tumors may be, and often are, not single, but multiple. 
Thirdly, that when a growth slowly infiltrates the tissues (this 
is seen particularly well in gliomata of the pons) the functions 
of the part affected may persist much longer than we should 
expect. 

Sites and Varieties of Cerebral Tumors. — There 
are hardly any parts of the brain in which malignant growths 
may not occur. These are mostly sarcomata of a mixed type, 
or the small-celled variety, peculiar to the nervous system, 
known as gliomata ; they are to be found most commonly in 
the cortex, cerebellum, and pons, also in the centrum ovale, 
basal ganglia, upon the cranial nerve-roots, in the pineal and 
pituitary bodies, or growing from the dura mater. Infiltrat- 



CEREBRAL TUMOR. 277 

ing glioma of the pons occurs in children ; the organ 
becomes enlarged and nodular, yet may still preserve its 
general shape. Sarcomatous growths of the brain are generally 
primary, and they do not (perhaps because they have not time) 
give rise to secondary growths elsewhere. Carcinomata of 
the brain are less common, and almost always secondary to 
growths in other parts of the body. 

Tubercular tumors occur as caseous masses, sometimes large 
and solitary, sometimes smaller and multiple ; they are com- 
monest in children, though not unknown in adults. The 
cerebellum and pons are favorite seats for them. They may 
give rise to no symptoms, while thoroughly quiescent ; or 
symptoms may rise and quiet down again. They may, on 
the other hand, slowly progress to a fatal issue; or again, a 
tubercular meningitis or a general tuberculosis may arise in 
connection with them and cause death. 

Gummata affects the surface of the brain rather than the 
deeper parts. 

Diagnosis. — The gradual development of symptoms and 
the presence of optic neuritis distinguish a tumor from 
cerebral hemorrhage and from most cases of softening. But 
it may happen in a very vascular tumor that a vessel suddenly 
gives way; and the symptoms due to this occurrence may be 
the first really to attract attention ; a careful inquiry into the 
patient's antecedent condition must be made ere a diagnosis 
can be formed. 

An abscess may be difficult to distinguish from a tumor. 
If the predisposing causes of abscess (ear disease, bone disease, 
injury to the head, etc.) do not exist, and have not been 
in operation, this militates against that diagnosis. In cerebral 
sarcomata, it must be remembered, there is often a history of a 
blow on the head. An abscess situated in the temporo-sphe- 
noidal lobe may remain latent a long time and then give rise 
to severe symptoms, such as coma, etc., whereas in most tumors 
the initial symptoms are better marked and the progress of 
24 



278 NERVOUS DISEASES. 

them more steady. Perhaps, too, optic neuritis is commoner 
in the early stages of tumor than of abscess. 

Treatment. — It is evident that in cases of malignant 
tumor little can be expected from purely medical treatment. 
It will be right, however, to give iodide of potassium at once, 
and increase the dose to 20 or 30 grains three times a day or 
more. For as a rule we cannot be certain that the disease is 
not syphilitic ; if it is, prompt treatment may arrest or cure 
it ; if not, no harm will have been done by such treatment. 
It is just possible, indeed, that growths other than syphilitic 
may thus be influenced for good. Where we suspect tuber- 
cular disease, cod-liver oil, iodide of iron, or other tonics, 
with a generous diet, must be given ; tubercular disease is not 
necessarily aggressive, and an improvement in the patient's 
nutrition may perchance arrest its growth. 

Lately, some cerebral tumors have been successfully dealt 
with by trephining the skull and removing the affected part 
of the brain. Some requisite conditions for such operations 
are the following : that the tumor should be single, situated 
superficially, in a part of the brain which can be reached by 
trephining and which can be operated upon without danger 
to life ; and, further, that the symptoms should be definite 
enough to fix the exact site of the disease and the requisite 
position of the trephine-hole. The motor area of the cortex 
is perhaps the only position for a tumor which satisfies these 
conditions. The feasibility of the operation proposed, the 
amount of risk which in the opinion of the surgeon it will 
involve, the prospect of complete or partial ablation of the 
tumor and of cure or relief for the patient's symptoms, are 
further questions which must be well weighed for each 
particular case. The possibility of a multiple tumor must 
also be remembered. If medical and surgical treatment alike 
fail us, attention must still be given to the nutrition and 
nursing of the patient. He may be fed with the nasal tube 
when unable to take food in the ordinary way ; and this, with 



CHRONIC HYDROCEPHALUS. 279 

attention to the state of the bladder and the prevention of 
bedsores, may keep him alive long after consciousness has 
failed. 

Chronic Hydrocephalus. — By chronic hydrocephalus 
is meant a gradual accumulation of fluid within the cranium, 
and in most cases within the ventricles of the brain. The 
causation of this is not always clear. In some cases it seems 
evidently due to pressure on the venous channels which take 
the blood from the brain, as when a cerebellar tumor presses 
upon the veins of Galen, or to closure of the apertures whereby 
the cerebro-spinal fluid normally escapes from the ventricles 
into the sub -arachnoid space, as when a meningitis at the 
base of the brain has sealed the foramen of Magendie. But 
sometimes no such mechanical cause can be found, and we 
have to suppose that there has been excess of secretion, 
probably inflammatory, from the lining membrane of the 
ventricles. This membrane, indeed, may be thickened, some- 
times even blocking up the Sylvian aqueduct (so that the 
mechanical factor is re-introduced) ; and, moreover, the 
character of the fluid, which in certain cases contains more 
albumen than does ordinary cerebro-spinal fluid, seems to 
indicate that some further process had been at work than the 
mere penning up of the normal secretion. 

The effects of such an accumulation of fluid, if large, is to 
arch the corpus callosum upward, rendering it tense and 
thin, to flatten out the floor of the third ventricle, pressing 
the large ganglia downward and outward, and to convert the 
lateral ventricles into large arched chambers over which the 
cortex and white matter is stretched in the form of a thin 
layer, from the outer aspect of which the natural sulci have 
been long since obliterated. The pressure affects the skull 
too, and mostly in a manner that is visible during life, for 
the disease, more often than not, begins before thorough 
ossification has taken place. 

Indeed, it may begin before birth ; hydrocephalus in the 



280 NERVOUS DISEASES. 

foetus forms one of the recognized causes of difficult labor. The 
fontanelle is rendered gaping and tense ; the bones on each 
side of the sutures begin to open out "like the petals of a 
flower," and the head enlarges, laterally and antero-pos- 
teriorly rather than upward, so that it appears somewhat 
flattened in relation to its size. The orbital plates are driven 
downward by the pressure and the eyeballs forced forward, 
so that the upper lid no longer partially covers the cornea, 
but leaves a ring of sclerotic exposed above it. This gives 
a staring look, which, with the bulging forehead above and 
the relatively small face below, is very characteristic of a 
hydrocephalic child. The skin over the enlarging cranial 
vault may become tense and thin and the superficial veins 
enlarged, the hair scanty. Sometimes the stretching of the 
brain-tissue and of the cranium becomes so great that the 
head becomes translucent, like a hydrocele. The enlarge- 
ment is not always symmetrical on the two sides, and some- 
times one part of the head may enlarge more than others. 
Irregular ossification may go on, so that Wormian bones are 
found in abnormal places, perhaps in the centre of an arrested 
suture. 

The mere enlargement of the head may sometimes cause 
inability to sit or stand upright, or even to hold it up without 
support. But there are other symptoms dependent on dis- 
ordered function. Fits are one of the most common ; among 
others are inability to walk and to use the hands properly, 
or actual paralysis with increased tendon-reactions, or even 
rigidity of the limbs ; blindness, with optic atrophy, squint, 
nystagmus ; deafness sometimes, irritability, the impairment 
of intellect, or complete idiocy. A rapid increase of fluid 
may lead to fatal coma. 

The prognosis is not good ; yet the disease may come to 
a standstill, and there are well-known instances in which the 
patient has lived to adult life (or even old age), and that 
with his full share of intellectual power. As to medical 



SYPHILIS. 28l 

treatment, mercury has been recommended, especially pills 
of mercury with squill (Watson), iodides, cod-liver oil, and 
tonics generally ; and in the way of surgical relief, cautious 
tapping through the distended suture with a fine trocar and 
cannula; or mechanical support and pressure by means of 
bandages or strapping to the skull. 

Hydrocephalus may come on in adult life, either as a 
consequence of some other grave cerebral disease (meningitis, 
tumor, or the like), in which case the symptoms of the pri- 
mary disease preponderate ; or in rare cases it may occur 
primarily. In two such cases which the author recently 
examined in the post-mortem room of St. Bartholomew's, the 
symptoms during life were simply such as would suggest a 
cerebral tumor — viz., pain in the head, vomiting, and optic 
neuritis, but no such cause for the effusion could be found at 
the autopsy. 

SYPHILIS OF THE NERVOUS SYSTEM. 

We have had to make several allusions to syphilis of the 
nervous system : we must now consider this subject more 
particularly. 

Morbid Anatomy — Gummata. — There are several ways 
in which syphilis may affect the nervous system. Definite 
tumors (gummata, syphilomata) may form in it; they are de- 
scribed as consisting of three layers; the periphery is a zone 
of small lymphoid cells; within this is a ring of fibroid tissue 
and in the centre a structureless or caseating mass. Gum- 
mata may be extremely difficult to distinguish from tubercles : 
their interior is more vascular, and hence caseation is not so 
marked a feature; giant cells, though sometimes present, are 
not so common as in tubercles. The discovery of tubercle 
bacilli will, of course, settle the pathological diagnosis. Gum- 
mata can be absorbed and leave only an inert scar; this is 
much less commonly the case with tubercle. 

Syphilitic Inflammation. — Apart from definite tumors, 



282 NERVOUS DISEASES. 

we may find a syphilitic inflammation ; in this the tissues 
undergo an infiltration with the small lymphoid cells, and 
though these have not the definite massing or structure of a 
gumma, doubtless the process is essentially the same. Such 
syphilitic inflammation is common in the cerebral meningesand 
in those of the cord : the process is generally subacute and more 
or less local, herein differing from an acute general meningitis; 
it does not concentrate itself upon the base of the brain and 
Sylvian fissures with such uniformity as does tubercular 
meningitis, but may affect either the base or the convexity. 
The pia is infiltrated with a somewhat thick, dirty-looking 
lymph, and the peripheral parts of the underlying nerve- 
tissues are apt to be affected as well. Syphilitic infiltration 
also may occur in the nerve- trunks and nerve- roots, particu- 
larly the cranial nerves. The nerves are thickened or show 
fusiform swellings, and appear gray or reddened according to 
their state of vascularity : microscopically they show accumu- 
lations of the small round cells in their interior, probably with 
abundant blood-vessels, while the nerve-tubes are in various 
stages of disintegration. 

Nodes. — In these two processes, syphilomata and syphi- 
litic infiltration, we have examples of syphilis attacking the 
nervous system directly. The attack may be rather more 
indirect. Thus, patches of subacute inflammation may form 
in the dura mater, analogous to the nodes that are seen out- 
side the skull ; if these occur at the foramina, where nerve- 
trunks leave the skull, the nerves are likely to be compressed 
and paralyzed. Perhaps, too, such nodes, if large enough, 
may irritate the subjacent cortex cerebri and so cause con- 
vulsions, etc. 

Arteritis. — But of far more importance than such nodes 
in its influence on the nervous system is syphilitic disease of 
the arteries. This is particularly frequent in the arteries of 
the brain — the basilar artery, circle of Willis, carotids, and 
sometimes their meningeal branches. The main character- 



SYPHILIS. 283 

istic of the disease is an overgrowth of the tunica intima, or, 
more strictly, of the deeper layer of it which lies between the 
epithelial lining of the interior surface and the fenestrated 
coat of Henle. This part of the coat is thickened with a 
material which appears to be partly fibroid, partly cellular. 
The thickening is sometimes in nodules, sometimes runs all 
round the vessel, and takes place at the expense of the lumen, 
so that it projects inwardly and narrows the calibre of the 
vessel. The narrowing may be so great as practically to 
occlude the vessel, or to cause occluding thrombi to form. In 
addition to this affection of the intima (end-arteritis) there is 
generally an infiltration of the external coat (peri-arteritis) 
with the vascular growth of small round cells which we 
have already noticed in connection with syphilis. Syph- 
ilitic arteritis appears to the naked eye as nodular thickenings 
of the vessels; these are isolated, and do not involve the 
arteries so generally, as does atheroma, neither do they 
become calcareous, as does atheroma. The effect of such 
disease may be varied and widespread. The loss of elasticity 
and partial occlusion of the arteries may cause a semi-starvation 
of the brain, producing variable phenomena of irritation and 
paralysis ; complete occlusion may produce necrotic softening 
with permanent paralysis as its result. Again as the distribu- 
tion of the arteritis varies so will that of the nervous lesions 
resulting from it ; and the particular symptoms will be as 
variable as the seat of the lesions. 

Degenerations and Neuroses. — There is yet another 
way in which syphilis acts as a cause of nervous disease ; that 
is by producing, or perhaps we should say predisposing to, 
chronic degenerations and functional nervous affections. 
Statistics make it almost certain that syphilis is in some 
way concerned in the production of tabes dorsalis, and in 
that of general paralysis to some extent ; again, it may be a 
factor in some cases of peripheral neuritis; but we do not 
know how. For in the morbid anatomy of such diseases we 



284 NERVOUS DISEASES. 

find nothing characteristic of syphilis, neither do the symptoms 
respond quickly and certainly to antisyphilitic treatment. We 
must content ourselves therefore with the vague supposition 
that they are the outcome of a vicious state of system which 
syphilis has contributed to produce. The same must be 
said of the syphilitic neuroses, epilepsy and neuralgia in 
particular, which have been described (doubtless with reason) 
by some authors. 

Diagnosis of Nervous Syphilis. — But omitting this last 
and very difficult question, how can we tell that a patient's 
nervous symptoms are due to syphilis ? Mainly by consider- 
ation (1) of the evidence of past or present syphilis ; (2) of 
the symptoms themselves — their character, development, and 
grouping ; (3) of the effect produced on them by antisyphilitic 
treatment. 

(1) The presence or history of syphilis does not, of course, 
prove the nervous disease to be syphilitic, but it is a step 
in that direction. We must either prove or assume the 
existence of syphilis. The primary infection has often been 
unnoticed or forgotten by the patient, for it may have been 
long ago ; and from many women it may be (as has well been 
said) "cruel and useless" to ask for such a history; we have 
then to rely upon later evidences. For information upon this 
head we must refer the reader to treatises on constitutional 
syphilis, only reminding him of the importance of looking for 
syphilides, scars on the legs, nodes on the skull and tibiae, 
affections of the tongue and throat, perforating ulcers of the 
palate, and choroiditis. The history, in married women, of 
a series of miscarriages without obvious cause has some 
diagnostic value. 

The nervous symptoms have no special connection with the 
severity of the original syphilitic symptoms. They may 
follow a severe or mild attack of syphilis. Indeed, it often 
happens that the only history obtainable is that of a chancre, 
with none of secondary symptoms. It may be that in these 



SYPHILIS. 285 

mild cases there has been absence or insufficiency of treatment, 
and hence the nervous sequelae. As to time, it is most 
common for nervous phenomena to appear at a late period of 
constitutional syphilis, it may be some years after the infection, 
so that they are commonly ranked as "tertiary" symptoms. 
But this is not invariable; the nervous system may be attacked 
within a few months, and while so-called "secondary" 
syphilides are in bloom. Syphilitic meningitis and diffuse 
inflammations of the nerve-roots, etc., are more likely to appear 
early than are gummata and arterial disease. 

(2) The nervous symptoms themselves. 

Their outbreak may be attended with some such conditions 
as these : a cachectic state described by Buzzard, in which 
the patient appears anaemic, sallow, and earthy-looking, as he 
would after long-repeated ague ; headaches, continuous and 
severe; pains in the bones of the legs and skull, severe and 
aggravated at night ; giddiness or paralysis, which may be in- 
complete and transient, in the district of the cranial nerves ; 
particularly ptosis and ocular palsies. Such preliminaries, 
however, are by no means necessary ; grave nervous affections 
may appear in a patient who has made no previous complaint. 

We cannot single out any symptoms as absolutely charac- 
teristic of nervous syphilis, for the disease acts by producing 
local lesions, whose clinical expression is the same, whatever 
their cause. Yet they may be suggestive of some of the 
syphilitic processes we have described. If the symptoms of 
cerebral tumor develop somewhat rapidly in a syphilitic sub- 
ject, we naturally think of a gumma. Epileptiform fits with 
double optic neuritis are common under such circumstances, 
for gummata specially affect the surface of the brain. Again, 
they are frequently small and do not create much inflamma- 
tion in their neighborhood, hence their effects may be local- 
ized within narrower limits than those of other tumors. Thus 
a hemiparaplegia may indicate a gumma involving one-half 
the cord, or a paralysis of one external rectus oculi, coupled 



286 NERVOUS DISEASES. 

with paralysis of the limb on the other side, may indicate a 
gumma at the egress of one sixth nerve. Cerebral symptoms 
of a more diffuse character, such as convulsions, which are 
unilateral, but have no definite place of commencement nor 
definite march, may very likely be due to a meningitis. The 
symptoms of a syphilitic meningitis are less acute than those 
of an ordinary purulent meningitis, neither have they the 
regularly fatal progress of the tubercular disease. Paralysis 
of nerve-trunks is a frequent occurrence in syphilis of the 
nervous system. It may be due to a syphilitic infiltration of 
the nerve, and is most frequent in the cranial nerves. It may 
be bilateral ; thus both third nerves or both facial trunks may 
be paralyzed. Such symmetry indicates a constitutional 
cause. Sometimes the grouping of nerve paralysis suggests 
disease of the orifice through which several trunks pass ; thus 
we may have paralysis of the facial and auditory of one side 
from periosteal swelling around the meatus auditorius internus, 
or paralysis of the oculo-motor nerves and the fifth from 
disease near the cavernous sinus or sphenoidal fissure, or 
unilateral paralysis of the tongue, palate, and vocal cord, 
when the hypoglossal and spinal accessory are implicated in 
syphilitic disease at the base of the brain. It is not very 
common to find syphilitic disease of the nerve-trunks of the 
limbs. Arterial syphilis may exhibit both general and local 
symptoms. There is generally headache ; faints, giddiness, 
and transient convulsions may occur. These are thought to 
be caused by interruptions in the equability of the blood- 
supply, from damage to the elasticity of the vessels, or from 
partial occlusion of them. Transient paralyses may in 
like wise happen, either of a limited area, such as the eye- 
muscles or face, or else a hemiplegia. A peculiar state of 
hebetude has been described. The patient is not actually 
comatose, but somnolent. He can be roused perhaps when 
pressed with questions, or sufficiently to take his food, but he 
soon relapses into stupor. This condition may last for days 



SYPHILIS. 287 

or longer ; sometimes it clears off for a short time and then 
comes on again. Even these symptoms, vague as they are, 
may not be present, and the first fact indicative of syphilis of 
a cerebral artery may be an attack of permanent hemiplegia 
caused by thrombosis and consequent cerebral softening. 
The syphilitic origin of such a hemiplegia can only be arrived 
at by excluding other causes. Embolism may be excluded 
when the heart and vessels appear to be healthy ; thrombosis 
from atheroma, and cerebral hemorrhage, when the patient 
is under middle age and has no renal disease. 

More characteristic than the individual symptoms is the 
grouping of them. There are not many conditions other 
than syphilis in which several organic lesions arise at divers 
parts of the nervous system. Hence, when the symptoms 
point to multiple lesions, it is probable that these may be 
syphilitic. Say that a patient who is paraplegic develops epi- 
leptoid fits with optic neuritis, or paralysis of some cranial 
nerves, or that a hemiplegia is complicated by symptoms dis- 
tinctly spinal, we cannot explain his condition except by sup- 
posing more than one focus of disease, and for these syphilis 
is a likely basis. We must remember, however, that malig- 
nant new growths are sometimes multiple in the brain, though 
not usually in both brain and cord, and that a very wide- 
reaching influence is exercised by such diseases as tabes dor- 
salis, general paralysis, multiple neuritis, occasionally tubercle, 
still more by disseminated sclerosis and by hysteria. Care 
and experience are therefore necessary to form a judgment 
from such data 

(3) The effect of treatment and the evidence of past organic 
lesions which have been arrested may confirm the diagnosis. 
Upon active syphilitic processes iodide of potassium given in 
sufficient doses has a more prompt effect than on any other 
form of disease ; so that when the progress of nervous disease 
is checked or reversed by the action of this remedy, the fact 
may be reckoned as confirmatory evidence of syphilis. The 



288 NERVOUS DISEASES. 

same may be said of mercury. We must of course assure ourselves 
that the disease is progressive and its subsidence spontaneous. 
For instance, a hemiplegic attack maybe treated with iodides 
from the commencement, and progressively improves ; but 
this proves nothing, since the natural tendency here is toward 
improvement. 

We cannot maintain the converse proposition, that where 
antisyphilitics do not cure, the disease is not syphilitic. They 
will not cure when there has been destruction of nerve-tissue, 
as when a gumma has destroyed the cerebral cortex, or soften- 
ing has taken place in consequence of arterial thrombosis. 

Treatment. — As to the treatment of cerebral syphilis and 
nervous syphilis in general, where symptoms arise which we 
conclude, or even reasonably suspect, to be due to syphilis, 
the patient should be immediately and energetically treated 
with iodides or mercury, or both. Iodide of potassium in 
large doses is said to act more quickly than mercury. Ten 
grains three times daily should be given at once, and the dose 
rapidly raised to twenty or thirty grains ; or in urgent cases we 
may begin with the larger doses. It is important often to gain 
time and catch up the disease (so to speak) before tissue has 
been destroyed which cannot be replaced. Even larger doses 
have been given. The drug may be given by enema if the 
patient cannot take it by the mouth. Treatment by iodide 
should be supplemented by treatment with mercury. This 
may be given in any of the usual ways: inunction is often a 
convenient plan. It is advisable to give a prolonged course 
of mercury, even in cases where a cure is apparently rapid ; 
for lesions may exist (such as arterial disease) without obvious 
manifestations, and relapses have to be obviated as far as 
possible. 

It is no exaggeration to say that by prompt and sufficient 
antisyphilitic treatment, in an early stage of the disease, life 
and eyesight and use of limbs have been saved. In cases of 
longer standing such good results cannot be expected ; for 



HEREDITARY SYPHILIS. 289 

probably the disease will have advanced beyond the stage of 
deposit to actual destruction of nerve-tissue. This we can- 
not repair, nor stop the secondary degenerations that may 
follow it ; but we may still perhaps, by antisyphilitics, remove 
deposits, relieve pressure on cells and fibres, or at least pre- 
vent the occurrence of further mischief. 

Mercury is said to be efficient in some cases upon which the 
iodides produce no effect. In arterial syphilis it is said to be 
decidedly the better drug. It is also said that after prolonged 
treatment with iodine patients become so saturated with it 
that it loses all curative or preventive powers. The general 
conclusion would seem to be that we should use iodides to 
make a first and quick impression on the disease, and a mer- 
curial course to ensure permanent benefit. 

For other methods of treatment, such as Zittman's method, 
hydropathics, the Aix treatment, etc., we must refer our 
readers to larger works. 

Nervous Disease from Hereditary Syphilis. — In 
hereditary syphilis nervous affections occur which anatomi- 
cally, at any rate, correspond to those of the acquired disease. 
For instance, there may be gummata of the brain, infiltra- 
tions of the nerve-roots or of the meninges, or even arterial 
disease. Sometimes we find in children, apparently as a 
result of hereditary syphilis, a diffuse induration of the cortex 
cerebri, and occasionally of the deeper parts of the brain and 
the cord also. This is caused by the growth of a fibroid 
tissue ; atrophy of the cortical cells and other nerve elements 
takes place. In hereditary syphilis gummata of the cord and 
local softenings of the cord are said to be rare, common as 
they are in acquired syphilis. The commonest clinical 
manifestations are these : convulsion-fits, either unilateral and 
presumably due to a meningeal lesion, or general, like those 
of true epilepsy; hemiplegia, or sometimes a "cerebral 
di-plegia ; " paralysis of cranial nerves. In a rare case wit- 
nessed by the author, a young woman with hereditary syphilis 



29O NERVOUS DISEASES. 

exhibited a fusiform swelling upon one median nerve with 
paralysis in the district supplied by it. She afterward had some 
epileptiform convulsions. Syphilitic children may become 
the subjects of a progressive dementia, the development of 
which is not unfrequently attended by fits or by hemiplegic 
attacks. In cases of this kind has been found post-mortem 
the induration of the nerve-centres, which we have just 
noticed. It may be combined Avith meningitis or arterial 
disease, or may stand alone. Lastly, it is not impossible that 
syphilis in the parents may contribute to the production of 
neuroses and nervous degenerations in their offspring; but 
this is a subject on which we know but little. 



CHAPTER VIII. 

DISEASES OF WHICH THE ORGANIC 
BASIS IS NOT KNOWN. 

We must now pass to a large and important class of dis- 
eases, which differ from those we have hitherto considered in 
the fact that their morbid anatomy is unknown to us. Some 
of them, indeed, have such definite symptoms and so definite 
a course as to indicate an organic basis not yet discovered ; 
of others (and notably those which are commonly called 
"hysterical"), the manifestations are so varied and capable 
of such rapid change, that we can hardly hope to trace back 
the perverted nervous activity to any structural change. 

EPILEPSY. 

The Epileptic Fit. — In epilepsy the most striking fea- 
ture is the "fit." Let us describe briefly an epileptic fit. 
The patient, who may appear to be in good health, suddenly, 
or after some slight warning, loses consciousness and falls, 
uttering, it may be, a peculiar cry as he falls. His face is pale, 
his eyes open and staring, perhaps rolled upward or sideward ; 
his limbs and face are contorted and for the moment fixed, and 
his breath held ; then the face becomes blue, and gradually 
the fixed spasm gives place to a series of convulsive move- 
ments. These again pass off, and in some two or three min- 
utes from the commencement he is lying deeply asleep and 
exhausted. The tongue is very frequently bitten; the ex- 
creta, especially the urine, may be passed under him. There 
are two other kinds of " fit " with which we may contrast this. 

Other Types of Fit. — («) The epileptiform convul- 
291 



292 NERVOUS DISEASES. 

sion, or Jacksonian epilepsy. In this, as we have already- 
pointed out, the convulsions begin in a definite member and 
spread in a definite way; consciousness is not lost (if at all) 
till they have spread over a considerable area, so that the 
patient is a witness of his own fit ; a localized paralysis often 
succeeds the fit. Whereas in typical epilepsy consciousness 
is lost suddenly, quickly, and early; the muscular spasm is 
general from the outset, or at least follows no definite order ; 
and afterward, instead of a localized paralysis, there is a 
general paralysis in the shape of coma. (/9) The hysteroid 
fit. In this there may be a sudden and no doubt real loss of 
consciousness; but it would appear to be less deep; thus, in 
falling, the patient rarely injures herself, neither (as a rule) is 
the tongue caught by the teeth so as to be severely bitten. 
She can, moreover, be roused by the application of such 
stimuli as cold water and faradization. The convulsions are 
not mere muscular spasms, but movements which seem to be 
guided by some idea — scratching, biting, kicking, and the 
like. They may continue for much longer than true epileptic 
convulsions : an hour or more. The patient may regain con- 
sciousness suddenly and completely, without the post-epileptic 
sleep. The urine is not passed involuntarily, as a rule. The 
eyes are usually closed, and the lids resist when we try to 
open them. 

It is important to bear in mind these different kinds of 
"fits." The usual import of Jacksonian epilepsy we have 
already pointed out ; the prognosis and treatment of hysteroid 
fits may be quite different from that of true epilepsy. But, 
though such types exist, many cases will be found in practice 
of a mixed character, which it is impossible to put into one 
or the other category. 

Preliminary Phenomena — the " Aura." — We must 
consider further the epileptic fit and its accessories. The 
approach of a fit may be heralded for a day or two before- 
hand by changes in the patient's mental state, such as the 



EPILEPSY. 293 

access of forgetfulness, irritability, despondent feelings, or by 
a feeling of exhilaration and bien-etre ; or perhaps by startings 
or twitchings of the limbs. Or it may take him while in his 
usual health. In any case, the immediate warning, or " aura," 
is of more importance. For not every epileptic fit begins 
with absolute suddenness ; there is often some short prelimi- 
nary to the loss of consciousness. The " aura " is tolerably 
constant for each particular case, but in different cases is of 
very various kinds. It may consist of strange sensations, 
tingling, numbness, pain, etc., in a limb or limbs; twitching 
of a limb, or movements, beginning in a definite part (like 
those of Jacksonian epilepsy) ;* phenomena referable to the 
special senses, either so-called " crude " sensations of lights, 
colors, balls of fire, ringing and whistling noises, disagreeable 
tastes and smells, or more elaborate sense-phenomena, such as 
visions, spoken words ; visceral phenomena, such as palpita- 
tion, disagreeable feelings in the epigastrium, etc. ; mental 
phenomena, such as dreamy states, misty memories, feelings 
of having been in the same place or heard the same words 
before. The patient often states that the warning is " giddi- 
ness." On inquiry, we sometimes find that this means a feel- 
ing of faintness; but sometimes he means by it a true feeling 
of vertigo — that is, of movement. A feeling of turning round 
is the commonest ; and this corresponds to the fact that at 
the commencement of the fit the head and eyes often turn to 
one side, or the whole body may rotate round and round. 

Post-Epileptic States — Automatism. — In the period 
that immediately succeeds the convulsions, it has been noticed 
that for a brief time the tendon-reactions are absent ; they then 
quickly return and become exaggerated ; there may even be 
ankle-clonus. Deep sleep most commonly succeeds the epi- 



* When the aura gradually ascends up a limb, the fit can sometimes be 
averted by a tight ligature round the limb, or by the previous application 
of a circular blister. 



294 NERVOUS DISEASES. 

leptic attack ; but sometimes this is replaced by a state in 
which the patient goes through certain actions automatically, 
or again he may appear to be actuated by delusions, or may 
become delirious and violent. The automatic actions are 
often those which the patient is accustomed to in his ordinary 
life, such as washing, undressing, etc., but they may be far 
more complicated. It is in this post-epileptic state that 
patients have committed crimes, made false accusations against 
others, and done various acts of which they are entirely 
unconscious when they have completely recovered themselves. 
Such automatism is more common after the minor epileptic 
attacks called " petit-mal " than after downright convulsions ; 
indeed, many authors think that an epileptic may pass into a 
state of automatism without even an attack of " petit-mal; " 
it is then called the equivalent of the fit. After a severe 
epileptic attack, the patient has generally a headache and 
experiences a certain loss of memory and mental confusion. 

" Petit Mai " is an important factor in epilepsy. It is 
an epileptic fit shorn of its convulsions, and in which the loss 
of consciousness is reduced to an extremely short duration. 
The patient may simply turn pale, stare vacantly, twitch a 
little, drop what he is holding, and then recover himself. 
Or the attack may be so transitory as scarcely to interrupt him 
even in such elaborate actions as reading, playing an instru- 
ment, etc. There are many degrees of petit mal, so that 
patients themselves will classify their "sensations" and 
"turns" into slight and severe. We may reckon also as 
petit-mal those abortive attacks in which the aura, usually 
well known to the patient, makes its appearance, but the con- 
vulsion-fit does not follow. According to Trousseau, attacks 
of petit mal have a more pernicious effect on the nervous 
system generally than have the major attacks ; this may be 
because they are more frequently repeated. As we have 
stated, they are frequently followed by curious post-epileptic 
conditions. Petit-mal may precede, even by several years, 



EPILEPSY. 295 

the development of the typical convulsions ; this we should 
remember when called to treat obscure symptoms of giddi- 
ness, faintness, and anomalous sensations in young people. 
We should remember, too, in fixing the duration of an 
epilepsy, to ask whether the patient suffered from such symp- 
toms before he actually had fits. 

Some epileptics have fits only at night, or, indeed, in sleep ; 
and they may have no knowledge of these, except they find 
their tongue bitten, their bed wetted, or their limbs sore and 
wearied. Others have fits only after waking from sleep, and, 
therefore, chiefly in the morning; others in the day only. 
Or they may come according to no rule of time. 

Time and Frequency of Fits. — The frequency with 
which fits are repeated varies much, not only in different 
cases, but in the same patient. Perhaps it is most common 
to have long intervals, months or longer, at the commence- 
ment of a case, and as the fits are repeated they tend to 
become more frequent. In some cases a certain periodicity 
can be traced. Some patients will have none for many 
months, and then have them in batches. The "status 
epilepticus " is a condition in which the patient has a series 
of fits, entering upon a second fit before he is well recovered 
from the preceding. This is an alarming state of affairs, and 
death (which is not common as a direct result of epileptic 
fits) may occur in it. A want of regularity in the recurrence 
of the fits will not surprise us if we reflect — first, that the laws 
according to which the disease itself develops are practically 
unknown to us ; secondly, that many circumstances may act 
either as the determining causes of fits or as agents in warding 
them off. 

Causes which Favor or Prevent the Occurrence 
of Fits. — We will mention some of these circumstances, 
though we cannot speak with much generality, for the 
influence of his surroundings is a question that should be 
studied specially for each epileptic. All sources of irritation, 



296 NERVOUS DISEASES. 

mental and bodily, may favor the production of a fit. 
Examples are : dentition, gastro-intestinal irritation from 
indigestible food or from worms (in children particularly) ; 
genital irritation due to the onset of puberty, to menstruation, 
to coitus (sometimes), to masturbation ; injuries, particularly 
blows on the head, the irritation of old wounds and scars ; 
ear disease, changes of season and climate ; divers states of 
nutrition ; excess in alcohol ; mental states, such as worry 
and anxiety, fright, passion, excitement. The badly consti- 
tuted nerve-centres of the epileptic respond to the ordinary 
stimuli of life by a manifestation of his disease. Some condi- 
tions appear to ward off fits. During acute diseases they often 
cease. They may disappear while a suppurating wound or 
sore is open, to reappear when it closes. Practical use has 
been made of this fact by the application of setons for the 
relief of epilepsy. Many epileptic women are free from their 
fits during pregnancy. This may be due to the disappearance 
of menstruation, for fits are usually worse about the time of 
the menses. Abstinence from flesh food has been said to 
control epilepsy * 

Predisposing Causes. — The deeper-lying causes of epi- 
lepsy — those, namely, which produce the vicious state of 
nervous system which lies at the bottom of its manifestations 
— are difficult to discuss. It is probably a matter of inheri- 
tance in most cases. It is common to find in the ancestry 
or collateral branches of the epileptic's family a history of 
such neuroses as insanity, intemperance, hysteria, or epilepsy 
itself. The disease generally begins during the first half of 
life (say under thirty). Rickets in children favors the 

* A hospital patient volunteered the following statement: When he was 
in work and could get food, he became subject to fits; these caused him 
to lose his situations; he then became destitute and semi-starved, and the 
fits would disappear. According to Dr. Haig's views, the production and 
excretion of uric acid (largely determined by the amount of meat eaten) are 
factors in the production of fits, as of other nervous phenomena. 



EPILEPSY. 297 

development of infantile convulsions ; such convulsions may 
be repeated from time to time, thus passing over into 
ordinary epilepsy ; or a child may get rid of its convulsions, 
but at some later period become epileptic. Acute diseases, 
such as scarlet fever, may favor the development of epilepsy. 
Puberty is a not uncommon time for the outbreak of epilepsy, 
or a later time, say between seventeen and twenty-five. The 
disease then may commence during all the time that the 
nervous system is undergoing development, adaptation, and 
consolidation. It may commence, too, when the nervous 
system is breaking down through senility. When it com- 
mences during adult life, we should look for such extraneous 
causes as alcoholism, syphilis, or Bright's disease. 

Course of Epilepsy. — The course of the disease is not 
very regular. It is generally held that the longer the fits go 
unchecked, the more certain and frequent does their repeti- 
tion become. Their type may change from nocturnal to 
diurnal, from severe convulsions to petit mal, or reversely. 
Usually the patient's health is good in the intervals of the 
fits, while the disease is in an early stage. As the disease 
proceeds, the headaches and the loss of memory, which we 
have mentioned to be a temporary effect of the fits, become 
a source of permanent trouble. A deterioration of intelli- 
gence and character sets in ; he is apt to become more and 
more forgetful, and stupid ; despondent, irritable, suspicious, 
and impulsive. A chronic epileptic often has coarse features, 
with a downcast, dazed, or stolid expression. Some patients 
become such dangerous lunatics at the time of their attacks 
that confinement is imperative ; others become permanently 
insane. As to termination — death in a fit is not common, 
but it may result from injuries sustained in a fit ; many 
patients drift into asylums ; others continue chronic epileptics, 
till intercurrent disease terminates their lives. When once 
the disease is established, a complete and permanent recovery 
is not probable. A patient may, under favorable circum- 



298 NERVOUS DISEASES. 

stances, have such long intervals between his fits as to be 
practically well ; but it would be unsafe to say that he will 
be liable to them no more. 

Treatment. — In the treatment of epilepsy drugs play 
a considerable part. No one can doubt the favorable 
influence of bromides. Bromide of potassium is the salt 
generally given ; bromide of sodium or of ammonium, or 
a mixture of the three salts, may occasionally have advantages. 
We should find, if possible, the minimum dose that will 
control the fits (pot. bromid., gr. xv-xx, ter die, may be called 
an average dose), and administer this for a lengthened period. 
Say that at the end of a year there have been no fits, then the 
dose may be lessened, or the medicine given less often, and 
thus cautiously dropped. This of course presumes that the 
patient bears the medicine well ; luckily epileptics are 
tolerant of it, and can often take large doses for long periods. 
Its ill effects may be as follows : (a) The bromide rash, a kind 
of acne, often severe and pustular. The addition of arsenic 
may relieve this. (/?) The state called "bromism." The 
patient loses appetite and flesh, and becomes sleepy, listless, 
and lethargic. This may pass off when the bromide is 
stopped, though his fits may return. We must notice, how- 
ever, that the occurrence of fits, quite independently of 
medicine, sometimes seems to clear the atmosphere of an 
epileptic's mind. 

No drug can, upon the whole, compare with the bromides, 
but others may do good: belladonna (tinct. bellad., r^v-n^xxx, 
ter die) ; zinc salts (zinci valerian., gr. iij-gr. v) ; borax, gr. 
x-gr. xxx. Borax is said to influence some cases not amen- 
able to bromides ; * it may produce nausea and vomiting, or 
an eczematous rash. Nitro-glycerin has been recommended. 

As valuable adjuncts to bromide we may mention digitalis, 

* In some chronic cases, where bromide has been administered for long 
periods, I have found a change to borax do great good. 



EPILEPSY. 299 

belladonna, iodide of potassium, arsenic. Salicylate of soda 
has been recommended on the ground that it favors the 
excretion of uric acid.* No doubt some of these drugs enable 
us to minimize the dose of bromide. 

Petit mal is often very intractable ; and bromide certainly 
has far less control over it than over the severer fits. 

The general treatment of epilepsy is an important but wide 
question. Did we know, and could we control, all the 
exciting causes of our patient's fits, we might do much to 
cure him. A few general remarks may be made. Children's 
education should not be neglected, but they must not be 
pressed with examinations and the like ; a large and rough 
school is evidently an unsuitable place for them. Girls and 
boys must be carefully watched through those critical times, 
the onset of menstruation and puberty. Epileptics should 
cultivate regular hours ; should have a plain, wholesome diet, 
without too much meat and with little, if any, alcohol ; 
should avoid both constipation and violent purges; should 
aim at securing a quiet, uneventful life, free from excitement, 
yet regularly occupied, in some trade or profession if they 
can manage it ; outdoor work is the best for them, but the 
risk of sudden falls must be remembered. Marriage is no 
cure for epileptics, and as a rule they should be dissuaded 
from it, both on account of the increased anxieties and 
responsibilities it entails, and of the risk that they will propa- 
gate neurotic offspring. 

Little can be done for the patient during the fit itself, save 
such obvious precautions as preventing injury during the fall, 
preventing tongue-biting by slipping something between the 
teeth, such as a spoon, handle of a brush, etc., loosening tight 
clothing from about his neck, etc. The fit must run its course, 
and it is best not to disturb the after-sleep. For the status 
epilepticus it is right to try such remedies as these : inhalation 



* Vide footnote to p. 296. 



300 NERVOUS DISEASES. 

of chloroform, chloral, bromide of potassium in large closes 
(by enema if necessary) ; an ice-cap to the head. If there 
seems danger of exhaustion, the patient must be fed and 
brandy given, by the mouth or rectum. 

Chorea. — In St. Vitus' dance, chorea Sancti Viti, or 
briefly " chorea," the patient is subject to involuntary move- 
ments of the face, tongue, limbs, and trunk, sudden, abrupt, 
and generally variable ; not spasms of isolated muscles, but 
coordinate movements, as if from a reflex start, or a quick 
voluntary impulse on the part of the patient. The face 
grimaces ; the limbs, as has been aptly said, appear to be 
tossed about by some unseen agency. The movements may 
go on while the patient is lying still, or may interrupt him in 
the performance of voluntary actions ; they are worse while 
he is being watched or examined, and cease while he is asleep. 
In a mild case there may be little more than occasional 
twitchings of the face or limbs, difficult to distinguish from 
mere nervousness. The patient drops things involuntarily, 
and gets into trouble for awkwardness or carelessness. After 
protrusion of the tongue, he draws it back with a snap. There 
is a peculiar abruptness of voluntary movement and gesture. 
Cases often begin in such a way. From such mild manifes- 
tations there is every gradation up to wild, constant jactitation 
of the limbs and body, preventing sleep and feeding, and 
leading to serious injury or exhaustion. The movements 
may be limited to the face or one limb (which is important as 
suggesting the cerebral origin of the disease), to the face and 
limbs of one side, or they may be limited in area at first, and 
then become general. Where the movements are specially 
marked on the right side of the body, there are often diffi- 
culties of speech. 

The movements are the most striking and characteristic 
mark of the disease; but some other points must be noted: 
(i) Some few cases appear to be characterized by paralysis, 
rather than movement. This " choreic paralysis " generally 



CHOREA. 301 

affects one arm ; the limb is limp, not rigid ; there is neither 
exaggeration of tendon-reaction, wasting of muscle, nor 
change in electrical reaction. The onset is not sudden, but 
subacute, coming on in the course of a few days, or a week or 
two. These characters are almost enough to differentiate it 
from other forms of paralysis in young people, and on inquiry 
or close observation some evidence of twitching movements 
will probably be found. (2) Mental affection. In the pres- 
ence of the facial spasms and the abruptness of manner which 
form part of the disease, it may be difficult to judge of minor 
modifications of disposition and intelligence. Probably there 
is some slight mental disturbance in many cases ; in a few the 
patient becomes absolutely, though temporarily, insane. The 
disease has then been called "chorea insaniens. ' ' (3) In a large 
proportion of instances there is evidence of valvular disease 
of the heart. The mitral valve is much more frequently 
affected than the aortic. The murmur may be found on 
first examination, or may develop during the course of the 
disease. Permanent valvular disease, with secondary hyper- 
trophy or dilatation, may remain. Post-mortem, in the 
(unfrequent) event of death during chorea, a ring of tiny 
nodules (granulations) may be seen near the edge of the mitral 
valve, 

Chorea is a disease of children, before puberty of boys and 
girls alike, and of young women. Its antecedents and affinities 
are very interesting On the one hand, it appears due to agen- 
cies that directly affect the nervous system. Fright is the com- 
monest and best established of these causes ; mental strains of 
other kinds might be added. Thus, children preparing for 
School Board examinations, when ill-equipped in brain and 
body for such a task, break down in this manner ; and the cho- 
rea of pregnancy is apt to be most severe when the pregnancy 
has followed a seduction. Again, in the patient's family, or 
sometimes in the patient's self, we may expect a history of other 
26 



302 NERVOUS DISEASES. 

neuroses.* On the other hand, it is closely connected with 
rheumatism. Chorea may develop during acute rheumatism, 
or rheumatism during chorea; the same person may have at sep- 
arate times rheumatism or chorea ; and the affection of the car- 
diac valves is a common feature in both diseases. Again, if in the 
patient's own person chorea appears to stand alone, we yet may 
frequently find, on inquiry into the family history, that other 
members have suffered from rheumatism. It is not unreason- 
able to suppose that in many instances at least chorea and 
rheumatism are but different manifestations of some one 
diathesis. More precise explanations of the disease have, it is 
true, been attempted. One of these is the " embolic " theory. 
Starting from the fact of valvular disease, it is maintained that 
the disease is due to minute fragments of fibrin swept from 
the valves into the arteries of the cortex cerebri, and there 
forming emboli, the effect of which is to irritate the cortex. 
For this theory there is no anatomical evidence, and it will 
hardly explain the course of the disease. We must admit 
that as yet we do not know the exact causation of chorea. 

The movements of chorea may develop from the small 
beginnings which we have described, or they may arise some- 
what suddenly. Some cases recover within six weeks or so ; 
others recover imperfectly and continue for a long time subject 
to a mild form of the disease. Relapses are frequent. It is 
rare for death to occur, but in the severe cases this sometimes 
happens. 

Treatment. — Obviously it is advisable to put the patient 
in quiet and comfortable surroundings; the mere removal 
from a poor home to hospital may do much good. A case of 

* Some years ago, the author had under treatment a young man who 
suffered from epilepsy; the convulsions were largely unilateral. His fits 
passed off, and he was attacked by movements differing in no respect from 
those of ordinary chorea on that side. When this attack subsided his fits 
began again. 



TETANY. 3O3 

any severity must be put to bed ; and when the movements 
are very violent and uncontrollable, the bed must be so 
arranged that the limbs cannot be injured against its sides, 
nor the body be thrown out of it. Plenty of nourishing food 
must be given, finely cut up, or in a fluid form where masti- 
cation and swallowing are impeded, or by the nasal tube if 
necessary. Bad cases will need alcohol also. For such bad 
cases chloral administered in full doses appears to be the best 
drug ; in less acute and more persistent cases arsenic should 
be given, and that freely. Where arsenic fails, sulphate of 
zinc often does good. In anaemic, poorly nourished children, 
iron and cod-liver oil may be administered at the same time 
as the arsenic. 

" Hereditary " Chorea. — We may mention here a rare 
form of disease, characterized by movements like those of 
chorea, but which differs in the following respects. It attacks 
older people, males or females past middle age. Its develop- 
ment is more gradual, its course chronic, and it is generally 
thought to be incurable. It is often accompanied by a pro- 
gressive dementia. Lastly, it runs in families. It has been 
called "chorea of the adult," or " hereditary chorea."* 

Tetany. — Tetany (which has nothing to do with the graver 
disease, tetanus) is characterized by a peculiar tonic spasm 
of the hands, and sometimes of the feet as well. The fingers 
take a position mainly due to spasm of the interossei; the two 
most distal joints are in extension, and the metacarpophalan- 
geal joint flexed, while the points of the fingers and thumb are 
approximated so that they form a sort of cone ;f there may 
be also some flexion of the wrist. The spasms generally come 
on during sleep, they may pass off during the day to recur 

* Sometimes also " Huntingdon's chorea; " just as St. Vitus's dance is 
called " chorea of Sydenham." 

f The posture is usually compared to that which the obstetrician gives 
his hand in order to insert it into the uterus. 



304 NERVOUS DISEASES. 

the next night, or they may be continuous. A painful cramp 
accompanies them. Trousseau says that they can be brought 
on by pressure on the nerve-trunks or arteries of the limb, 
until the disease is extinct. Swelling on the back of the 
wrists is sometimes complained of. 

In addition to the actual spasm, we must notice : — 

(1) The phenomenon of " facial irritability. " If the finger- 
nail be drawn somewhat roughly across the facial nerve, where 
it crosses from the ear toward the eye, the eyelid blinks from 
a twitch of the orbicularis muscle. 

(2) There is, according to Erb, increased electro-irritability 
of the nerve-trunks generally, but without qualitative changes. 
This may not be easy to demonstrate. 

Tetany is most common in young children. In them it is 
accompanied by, and probably due to, rickets. In conjunc- 
tion with it, laryngismus stridulus often occurs ; sometimes 
also the child has convulsions. It is also seen in women, 
either in young women of hysterical temperament without 
other apparent cause, or in women who are debilitated by 
lactation.* Epidemics of tetany, probably of hysterical type, 
have been reported from girls' schools. Bromide of potas- 
sium, with cod-liver oil, and suitable dieting in the case of 
rickety children, forms an appropriate remedy. 

Paralysis Agitans. — A typical case of paralysis agitans 
will probably present the following features : The patient is 
usually in advancing years, of either sex, perhaps a man most 
commonly, and complains of weakness and tremor. The 
tremors, as we have already said, are rhythmical, rapid, and 
commonly small in amplitude ; they affect particularly the 
muscles of the thumb and fingers. The movement has been 
compared to that of making pills or rolling a cigarette. They 



* Tetany has also been ascribed to gastric disturbance (the disease has 
followed the operation of washing out the stomach), and to the removal of 
the thyroid gland. 



PARALYSIS AGITANS. 305 

may involve the wrist-joint and larger segments of the limb, 
and then produce a coarser flapping movement. They have 
this characteristic, that they are present while the patient rests 
the limb, and often (at least in the early stage) stop when he 
begins to use it. The legs may shake also, and the tongue. 
The head, according to some authorities, does not shake. 
Along with the tremor, and sometimes independently of it, 
there exists an embarrassment of movement producing the 
effects of paralysis, though there may not be actual loss of 
muscular power. The patient's aspect is peculiar. His face 
and eyes have an immobile look. His head is bent a little 
forward and held stiffly ; his trunk bent forward at the hips. 
His speech is deliberate ; his voice is sometimes piping, like 
an old man upon the stage (as Dr. Buzzard puts it), sometimes 
whispering. Sometimes he cannot walk without hurrying, 
as if he were trying to prevent himself falling forward. Some- 
times a peculiar phenomenon is seen : when he has once 
begun to walk he cannot stop himself; or, again, if given a 
push backward, he has to go backward until some obstacle 
stops him. He is often very sensitive to heat, and complains 
of spontaneous " flushes of heat." He may be tormented by 
a sense of restlessness both by night and by day, and is apt 
to be sleepless at night. He will sometimes say that he feels 
the tremor " internally." 

There is no affection of sensibility. The tendon-reactions 
are generally normal, sometimes exaggerated. The mind is 
usually unaffected, although the patient is (not unnaturally) 
disposed to be gloomy about himself; but in some instances 
insanity has developed. 

Among the antecedents of paralysis agitans we often find 
such influences as these : exposure to damp and cold, rheuma- 
tism, mental shocks, particularly fright, or prolonged mental 
strains as from failure in business, family troubles, and disap- 
pointments. Occasionally, though rarely, two or more mem- 
bers of a family suffer. As a rule, the disease begins gradu- 



306 NERVOUS DISEASES. 

ally: tremor is noticed in one hand, whence it may spread 
either to the leg, so as to assume an hemiplegic distribution, 
or to the other hand, and then to the legs. The tremor is 
sometimes preceded by pains in the limbs. In some instances 
the tremor gets less, but the weakness increases. Indeed, 
there are cases which exhibit no obvious tremor, and here the 
diagnosis may be difficult, the peculiarities of physiognomy 
and of gait being the chief guide. Some cases develop in the 
form of a paraplegia, with a very gradual onset, and without 
obvious causation. It is less common for the disease to begin 
abruptly, but this has been observed, especially after frights. 
The disease progresses slowly, but very surely ; the tremor 
becomes general, the weakness increases, till at last the patient 
cannot walk, cannot stand, and may lose the use of his hands. 
When once bedridden, he is liable to the complications of 
bedsores, cystitis, etc., unless he dies from some intercurrent 
malady. 

Treatment. — Treatment, it is to be feared, will do little 
to stop the disease; but, nevertheless, some relief may be 
obtained. Electricity, either in the form of the constant 
current or of static electricity, has done some good. Of 
drugs, iron in large doses, or nux vomica, or strychnia, un- 
doubtedly benefit some patients ; iodide of potassium or 
arsenic may also be given. 

Diagnosis. — A well-marked case is easy to recognize ; but 
in others there may be difficulty of diagnosis. The disease 
has to be distinguished from disseminated sclerosis ; the 
characters of the movements are different, there is no nystag- 
mus, and, as a rule, no excess of tendon-reactions, and the 
age of the patient is more advanced ; also from general 
paralysis, from hysterical tremor, from toxic tremors, as of 
mercury, lead, alcohol. What line can be drawn between 
the tremor of paralysis agitans and the tremor of senility is 
difficult to say. 

Writer's Cramp. — There is a class of nervous affections 



WRITER S CRAMP. 7>°7 

which have been called "neuroses of occupation," or pro- 
fessional "cramps," and which originate as follows: — In the 
course of a man's avocation he may be called upon to perform 
repeatedly, and for a length of time, some movement or 
movements of a highly specialized nature, such as writing, 
playing a musical instrument, working a telegraph, and so on. 
As a result the motor apparatus concerned in the movement 
breaks down, so that on attempting to perform it he is seized 
either by motor spasms or, it may be, by pains in the hand or 
arm, which prevent him from going on. There may be no 
loss of gross muscular power, no wasting or other sign of 
organic disease ; and for all other purposes except his par- 
ticular work his hand may be as useful as ever. The com- 
monest and most typical affection of this kind is that known 
as writer's cramp. This is apt to attack clerks whose business 
necessitates their writing many hours a day. Often the 
patients are poorly nourished, angemic people of a neurotic 
type or with neurotic family history. In such people writer's 
cramp may appear even with a limited amount of writing, say 
three or four hours daily. Some kinds of writing seem to 
favor its development more than others, those, for instance, 
on which the attention must be kept closely fixed — those which 
necessitate an uncomfortable position of the hand,* steel pens 
rather than quills, etc. An extra long bout of writing often 
determines the appearance of the disease. Then, whenever 
the patient sets about writing and has got through a few lines, 
he is either seized with a pain in the hand or arm which 
causes him to desist, or more commonly muscular spasm 
arises, his fingers assume a cramped position which renders 
further writing impossible, or spasmodic movements set in 

*Thus a post-office official with this affection informed me that a certain 
kind of writing in connection with the telegraph, in which the hand is kept 
in one place and not drawn along from left to right, as in ordinary writing, 
is particularly apt to set up writer's cramp. His statement was drawn from 
observation of his own case and that of several fellow-clerks. 



308 NERVOUS DISEASES. 

which may even fling the pen from his fingers. If the patient 
learns to write in such a way as to avoid the use of the small 
hand-muscles, say with movement of the wrist or elbow, or 
even with the left hand, it may happen that after a time the 
affection begins in the newly employed parts. This would 
seem to show that the disease is not merely a peripheral affec- 
tion, but that its cause is in the nerve-centres themselves. 
The best plan for the patient is to give up the occupation of 
writing. If this cannot be done, a temporary holiday should 
be secured, and the writing minimized subsequently. Atten- 
tion should be given to the general health. Local treatment 
of the following kind is advantageous : either massage (which 
is said to have effected cures), galvanization,* or moderate 
faradization of the hand and forearm, repeated regularly and 
frequently for a considerable time. 

Migraine. — Hemicrania, which name has been abbreviated 
into migraine or megrim, consists essentially of a paroxysmal 
headache, often limited (as the name implies) to one side of 
the head, with which headache other phenomena may be 
associated. The paroxysms may appear at regular intervals, 
such as a week or a month, or they may be quite irregular in 
their appearance. They often are determined by some such 
circumstances as these : overwork, irregularity in meals, indi- 
gestible food (from which cause and from the presence of 
vomiting migraine is often called "bilious headaches "), strain 
upon the eyes, exposure to bright lights. These last causes 
harmonize with the fact that visual symptoms are often present. 
Picture galleries and theatres are thus potent provocatives. 
But co-operating with these external causes there must be a 
predisposition on the part of the patient. The exact nature 

* This may be given after the plan recommended by Dr. Poore. A con- 
stant current is passed from shoulder to hand, and the patient is instructed 
to perform regular rhythmical movements of the hand and fingers during 
its passage. 



MIGRAINE. 3O9 

of this predisposition we do not know ; it may be that nervous 
instability, often inherited, which manifests itself in other 
patients as epilepsy* and other neuroses; it may be (as 
strongly urged by Dr. Haig) the gouty diathesis. Neither do 
we know the exact pathology of the paroxysm ; it has been 
ascribed to spasm and to dilatation of the cerebral vessels, and 
that grand deus ex machina, the sympathetic nerve, has been 
invoked for the explanation of this spasm ; again, it has been 
likened to the explosions of epilepsy taking place in a sensory 
sphere of the cortex. An attack may be heralded by drowsi- 
ness and depression, or occasionally with extreme irritability ; 
the pain in the head then begins, often in one definite spot, 
over one eye or in one temple, or at least upon one side of 
the head ; thence it radiates and may become general. Usually 
the migraine terminates in the course of a day ; sometimes it 
lasts two or three days. This may constitute the whole of the 
attack, but often there are additional symptoms. The com- 
monest is vomiting, which occurs usually toward the end of 
the attack, and therefore appears to relieve the headache. 
Visual symptoms are common also ; the patient may see flashes 
of light, colors, etc., or sometimes an elaborate zigzag of light 
forming a kind of fortification or battlement pattern; dark 
spots may appear in his field of vision, or he may become 
temporarily hemianopic. Less commonly the limbs are affected 
by tingling and numbness, anaesthesia, or motor paralysis, in 
the arm of one side, or having a hemiplegic distribution. 
There may be temporary aphasia. These forms of paralysis 
end with the attack. Another kind, which, although transi- 
tory, lasts longer thai^ these, is paralysis of the third or of the 
facial nerve of one side ; recurrent paralysis in these districts 

* It is stated by good authorities that epilepsy and migraine do not occur 
in the same subject. A patient attending at Queen's Square Hospital for 
typical migraine has described to me attacks which pass over into convul- 
sions with unconsciousness. Dr. Liveing and others recognize such an 
interchange between epilepsy and migraine. 



3IO NERVOUS DISEASES. 

seems often to originate in attacks of migraine. Sometimes in 
a severe attack of migraine the drowsiness and lethargy 
become so great as almost to amount to coma, so that were it 
not for the history of previous attacks we might be led to 
suspect a cerebral tumor. 

Treatment. — In a bad attack of migraine the patient 
should remain recumbent, in a darkened room protected from 
noise, and take only fluid food in small quantities at a time. 
Antipyrin should be given, say in ten-grain doses every hour, 
up to three or four doses ; its effect is usually rapid and satis- 
factory ; and the more so the earlier it is given in the attack. 
Other medicines are guarana, citrate of caffein, strong coffee 
or tea, alcohol. Our treatment of the case during the inter- 
vals must be guided by our surmises as to its causation. 
Country air, out-door life, iron and other tonics may be best 
for anaemic, ill-developed patients ; those with nervous 
heredity may have a course of bromides in small doses; 
alkaline bicarbonates with gentian or calumba, and attention 
to diet, benefit cases where digestion is at fault. 

The "Uric Acid Headache." — According to Dr. Haig, 
many cases of migraine are to be reckoned as a "uric acid" 
headache. The radical fault is the presence in the system of 
an excess of uric acid (we may say, the gouty diathesis). This 
may be either locked up in the tissues or pass into the blood, 
whence it is excreted by the urine. Such paroxysmal head- 
aches are marked by the fact that during the paroxysm there 
is an excess of uric acid in the urine. This makes it probable 
that they are caused by its presence in the circulating blood. 
They maybe relieved by the administration of acids (say a 
drachm of dilute nitro-hydrochloric acid in divided doses) ; 
which, rendering the blood more acid, drives the uric acid back 
into the tissue. But during the interval we should aim at (i) 
diminishing the production of uric acid, which is best effected 
by cutting off from the diet all forms of butcher's meat, malt 
liquors, and strong wines ; (2) aiding its excretion as fast as 



NEURALGIA. 3 1 1 

formed, which can be done by prolonged administration of 
salicylates, or alkalies. 

Neuralgia. — We have already alluded to the subject of 
neuralgia and the nerves (trigeminal, sciatic, cervico-occipital, 
intercostal) which it principally affects. The pain of neural- 
gia is often of two kinds : a dull continuous ache, principally 
in the site of the nerve-trunk ; or sharp, darting twinges, princi- 
pally in the peripheral distribution of the nerve. Both these 
kinds of pains, but particularly the latter, are apt to occur in par- 
oxysms, or at least to have paroxysmal exacerbations. The pain 
of a neuralgia, in the strict sense of the term, is limited to the area 
of a particular nerve, but as it gets worse its original distribu- 
tion may be concealed by irradiation to other parts. (Painful 
affections of many organs, for which no cause can be found, 
are often loosely spoken of as " neuralgia " of the uterus, 
kidney, etc.) Lastly, we speak of a simple neuralgia only 
where we have reason to believe that there is neither organic 
disease of the nerve itself, nor disease of the parts around 
directly invading or pressing upon it. It is. most important 
both for prognosis and treatment o ascertain that the neuralgia 
is not thus symptomatic of organic disease. Bilateral neural- 
gia suggests disease of the nerve-centres, or of the bones or 
membranes around the spinal nerve-roots. The causes of neu- 
ralgia, like those of many other neuroses, are partly reflex, 
partly constitutional. A source of peripheral irritation, in- 
volving the termination of a branch, may produce neuralgia 
either of that branch or of others, or sometimes even of more 
distant nerves. Thus, a face-ache may be dependent on bad 
teeth, while the patient has no pain in the teeth, and denies that 
there is anything the matter with them. Such reflex causes of 
neuralgia must be always looked for, since in their removal lies 
the best chance of curing the disease. We may enumerate 
among them carious teeth (by far the commonest cause of 
facial neuralgia); anomalies of refraction and overstrain of 
the eyes as a cause of frontal neuralgia ; inflammation of the 



312 NERVOUS DISEASES. 

nasal cavities, frontal sinuses, and of the ear in various neu- 
ralgia? of the face and head ; faecal accumulations, ulceration 
of the cervix uteri, etc., in neuralgia of the lower extremities. 
Exposure to cold may be the starting-point of a neuralgia. 
Among constitutional causes, the commonest is general anae- 
mia and mal-nutrition, which doubtless acts by setting up mal- 
nutrition of the nerve ; a neurotic predisposition (both causes 
are seen at work in delicate young women of an hysterical 
temperament) ; fatigue and sleepless nights, the gouty diathe- 
sis, an inveterate taint from malaria, or from syphilis. Con- 
stipation is a condition which should be inquired after and 
treated. The general remedies — the reader will apportion 
them to their appropriate classes — are proper feeding (with a 
moderate allowance of good wine), rest from work, change of 
air and scene, quinine (the drug of most general application 
in neuralgia), iron, bromides, alkalies with vegetable tonics, 
arsenic, iodides. In addition to this general treatment, and 
the removal of such sources of irritation as we may have been 
able to find, remedies for the neuralgia itself will always be in 
demand. There is a long list of such remedies — quinine, gel- 
semin, croton-chloral, antipyrin, citrate of caffein, alcohol, 
internally ; morphia by the mouth or subcutaneously ; local 
applications of great variety — fomentations, simple or with 
poppy-heads, menthol, chloral-camphor pigmentation, bella- 
donna, aconite, cocain, morphia ; counter-irritants — the gal- 
vanic current applied without make or break, and with the 
anode over the painful nerve. Lastly, in severe and obsti- 
nate cases, and particularly in the excruciating paroxysmal 
neuralgia known as "epileptiform neuralgia," or "tic dol- 
oureux," surgical aid may be invoked with the view either of 
stretching the nerve, of excising a portion, or even removing 
some of its deeply seated parts, such as Meckel's ganglion. 

Additional Symptoms. — In addition to the pain of 
neuralgia, there may be sometimes tenderness. This may be 
diffuse, spread over the whole area of the neuralgic pain ; but 



HYSTERIA. 3 I 3 

more commonly it is localized at certain points in the course 
of the nerve, chiefly those where it emerges from beneath 
bones and fasciae. These "tender points" we have already 
noticed. Sometimes an attack of neuralgia leaves a tempo- 
rary anaesthesia. Trophic changes are sometimes witnessed ; 
thus the hair may turn gray in the district of a nerve affected 
with neuralgia ; or an herpetic eruption may occur. The 
common affection, herpes zoster, or shingles, is generally pre- 
ceded by intercostal neuralgia. Trophic changes in the 
muscles, such as wasting with reaction of degeneration, point 
to a neuritis rather than a neuralgia. 

There are some important diseases affecting the nervous 
system, concerning which we believe it best to refer our 
readers to text-books on general medicine and surgery ; these 
are delirium tremens, tetanus, hydrophobia. Neither shall 
we discuss here the subjects of myxoedema, Graves' disease, 
Raynaud's discease, angina pectoris. 

Hysteria. — The name hysteria, though doubtless old- 
fashioned and faulty, is still generally employed to denote a 
certain type of disease, whereof we will try to enumerate a 
few characteristics, though we shall not attempt a definition 
of it. 

General Characters. — The disease occurs chiefly in 
women, most frequently of all in young women ; in girls and 
boys also; sometimes in men. It is not therefore necessarily 
connected with the uterus (as the name would imply) ; nor 
with the ovaries : nor, indeed, with the sexual system at all. It 
is essentially an affection of the central nervous system; but 
sources of peripheral irritation, particularly when seated in 
the sexual organs, may have a powerful influence in deter- 
mining its outbreak. The symptoms of the disease are very 
variable ; and they vary, not only in different patients, but 
in one and the same patient ; so that mutability of symptoms, 



3 14 NERVOUS DISEASES. 

sudden appearance and sudden disappearance of them, often 
suggests to us that they have an hysterical basis. It is, on the 
other hand, possible for hysterical symptoms to persist un- 
changed for years. The disease may present a remarkable 
counterfeit of other nervous diseases; and this not merely of 
such general affections as epilepsy, etc., but of local nervous 
disease such as hemiplegia, paraplegia, or paralysis of still more 
local origin. On this account the name " neuro-mimesis," 
or, anglice, " nervous mimicry," is sometimes applied to it. 
Yet it depends, so far as we can at present determine, on no 
actual organic lesion. Hence death from hysteria is almost 
unknown, and the presence of certain symptoms (which point 
to organic disease) may be taken as negativing the diagnosis 
of hysteria. Such symptoms are — optic neuritis, optic atrophy, 
reflex iridoplegia, bedsores and cystitis, electrical reaction of 
degeneration in muscles, complete and permanent absence of 
knee-jerk. We may go further, and say that the more closely 
the grouping and sequence of symptoms resembles that which 
would follow any local lesion, the less likely is the disease to be 
hysterical. Again, an emotional Or volitional element is often 
distinctly present. We do not mean that mere phychological 
states can produce bodily disease, but that the circumstances 
under which strong emotions develop may produce, or per- 
haps remove, hysterical manifestations; and that circum- 
stances under which the will becomes enfeebled or strength- 
ened, favor or oppose respectively the development of hysteria. 
Lastly, hysteria is a genuine morbid state ; it is not synony- 
mous with humbug. Hysterical patients, like others, and 
perhaps more often than others, may practice deception ; but 
this is no necessary part of the complaint ; it is often im- 
probable, and sometimes impossible, that they could manu- 
facture the symptoms they exhibit. 

Causation. — As in epilepsy, so in hysteria, the radical 
fault is nervous instability, whose exact nature is unknown to 
us. Such fault is, in the graver cases, often inherited : a family 



HYSTERIA. 3 I 5 

history of various neuroses may be elicited. It may be pro- 
duced also by a life of luxury and idleness, leading to ennui 
and concentration of the thoughts upon self; and hence it is 
commonly thought that young women of the better classes 
are the most frequent victims of the disease. But it may be 
seen under quite opposite conditions in poorly fed, anaemic, 
overworked subjects. Sudden shocks of all kinds — frights, 
disappointments, griefs — prolonged strains of anxiety and 
overwork, are potent factors in its production. It may follow 
or accompany other diseases, either as part of the mental and 
bodily debility which results from any severe and long illness ; 
or, it would seem, as a reflex result from disease and irritation 
of the pelvic organs ; or as an accompaniment of organic 
nervous diseases, such as hemiplegia, disseminated sclerosis, 
etc. Toxic influences produce it, alcoholism often, plumbism, 
and other such causes sometimes. Injuries may determine 
curious attacks of local hysterical paralysis, or a general and 
chronic form of neurosis which we shall describe later. 
According to Grasset, phthisis and hysteria have a close 
relationship ; the two diseases frequently appearing in mem- 
bers of the same family. 

Symptoms. — There is no definite course to a case of 
hysteria; sometimes one set of symptoms may be present, 
sometimes another. Even this feature of change is not 
invariable ; some symptoms (notably that of paraplegia) may 
remain unchanged and unaccompanied by others for a long 
time. Hence we can only make an enumeration of such 
phenomena as may in various instances be found ; they may 
be pieced together differently in different cases. 

Fits. — These vary much in severity. In a slight hysterical 
attack there is no loss of consciousness, only a burst of tears 
or laughter, or both alternately, with some jactitation of the 
limbs perhaps, and a choking feeling at the throat. Or, 
again, the patient may lose consciousness and fall, remaining 
for a short time limp and motionless, or perhaps rigid. Or 



316 NERVOUS DISEASES. 

there may be convulsions, so that the attack bears a general 
resemblance to epilepsy. We have already contrasted these 
"hysteroid" attacks with those of epilepsy : we will again 
enumerate a few points of difference. In hysteria the face 
does not turn pale or blue, and is not drawn as a rule ; the 
eyes are closed, not staring, the lids tremulous and resist 
opening ; the tongue is not bitten, there is less foaming at 
the mouth ; instead of uttering one solitary initial cry, the 
patient may scream, moan, or even talk throughout the attack ; 
the movements are apt to be violent, so that several people are 
required to hold the patient ; and purposive, not mere tonic 
and clonic, spasms ; and the face may at the same time assume 
expressions of fear, rage, etc. The movements may go on 
for a very considerable time ; the excreta are not passed 
involuntarily ; rapid recovery may take place, and though 
the patient may be exhausted afterward, the fit is not followed 
by the coma or the dazed mental condition so often seen in 
epilepsy. In spite of the fall and the violence, the patient 
usually sustains little real injury. The attack can often be 
cut short by appropriate remedies. In a long-continued 
hysterical attack the temperature does not rise to the height 
which it may reach in the "status epilepticus." 

Hysterical fits, like epileptic fits, may be preceded by an 
aura ; the most frequent warnings are sensations in the lower 
abdomen or epigastrium, palpitation, choking at the throat 
("globus"), vertigo, noises in the ears. 

Under the title of hystero-epilepsy, Charcot describes a 
still graver type of hysterical fit. This begins with an attack 
simulating true epilepsy — cry, loss of consciousness, tonic and 
clonic spasms, coma, perhaps even tongue-biting ; next follows 
a period of wild and extravagant movements and postures, 
sometimes called "clownism." Opisthotonos is frequent, 
or an attitude like that of crucifixion. This passes into a 
stage wherein the patient expresses by action and gesture 
emotions such as fear, hatred, love, sometimes even acting 



HYSTERIA. 317 

out by voice as well as gesture some drama connected with 
her life-history. In the final stage she has hallucinations, 
seeing spectres, rats, and other objects which terrify her ; 
and the attack may leave her hemiplegic, hemianassthetic, 
with contractures of a limb or limbs, etc. Fully developed 
hystero-epilepsy appears to be unfrequent in this country. 
Lastly, it would seem that in some few cases, apparently 
purely hysterical, attacks may occur consisting of convulsions 
limited to one limb or part of it, without loss of conscious- 
ness, so as to simulate " Jacksonian epilepsy." Probably 
such convulsions will have a less definite order of spread ; 
and if there be optic neuritis, mere hysteria will of course be 
negatived. 

A fit which can be provoked by touching or pressing some 
definite part of the body is more often than not hysterical. 

Motor Paralyses. — Hysterical hemiplegia may come on sud- 
denly after a fit, or gradually. It usually affects the limbs 
only, not the face or tongue, neither (when right-sided) is 
there true aphasia. The paralyzed limbs may be limp, or 
there may be contracture; if contracture be present it prob- 
ably develops pari passu with the paralysis, and is not (as 
usually in organic disease) a late phenomenon. Hysterical 
paraplegia, like hemiplegia, may be sudden or gradual in 
development, flaccid or rigid in character. If both lower 
limbs be paralyzed, without trace of rigidity, the knee-jerks 
normal or somewhat exaggerated, the muscles well nourished 
and normal in their electrical reactions, we have a condition 
(as pointed out by Dr. Buzzard) which tallies with no known 
organic disease, and is therefore probably hysterical. Un- 
fortunately, the legs in hysterical paralysis are very often rigid, 
and then it may be quite impossible to diagnose between 
hysteria and disease of the dorsal cord with descending scle- 
rosis; the more so because such hysterical paraplegia may be 
a very permanent symptom, and may stand alone without 
other manifestations to guide us. Hysterical paralysis may 
27 



3 l8 NERVOUS DISEASES. 

spread from one limb to another, becoming more or less 
general. In such cases it is not unusual to find that the 
right hand is spared, so that the patient can feed herself and 
help herself to a certain extent. Paralysis of one limb only 
(monoplegia) is not unfrequent. This is often accompanied 
by contractures, and by anaesthesia of the limb. It is per- 
haps most frequent after some injury to the limb, and con- 
stitutes a kind of local hysteria. 

Motor spasms of one kind or another are very frequent in 
hysteria. Involuntary jerks of the limbs are often seen ; 
sometimes there is a condition resembling chorea ; some- 
times one or both hands are affected with regular rhythmical 
flapping movements ; sometimes there is a fine tremor seen 
when the hands are held out. The typical tremor of dissem- 
inated sclerosis, which begins when the patient endeavors to 
use her hand, causing large irregular wavy movements, and 
ceases again when the voluntary movement is completed, 
does not, according to Buzzard, occur in hysteria. This is 
an important observation, since the two diseases are often 
difficult to diagnose, and indeed may be commingled in one 
and the same patient. Hysterical contracture or rigidity is 
common. Thus we may have a paraplegia or a hemiplegia 
with rigidity \ or one upper limb may become useless, anaes- 
thetic, and rigid at all the joints, while the fingers (in partic- 
ular) become tightly flexed into the palm. Or the fingers of 
one or both hands, and sometimes even the toes, may become 
thus flexed without any obvious palsy of other segments of 
the limbs. Fibrous adhesions about the joints may form 
when hysterical rigidity is long continued. 

Affections of Sensation. — Anaesthesia may occur in scattered 
patches, or, like motor palsy, be paraplegic, hemiplegic, or 
monoplegic in distribution. When it affects one limb (it 
often, as we have said, occurs along with paralysis and con- 
tracture of one upper limb), it involves the whole of the digits 
and the various segments from periphery to root, like a 



HYSTERIA. 3I9 

stocking or glove, according to the plan of cortical anaesthesia 
(vide p. 109). Hemianaesthesia involves one half the body, 
face, and scalp, with the limbs and special senses of the same 
side (as if from disease ot the posterior part of the internal 
capsule). 

Anaesthesia may exist in various degrees; its existence 
may be unknown till the physician has looked for it. 

Analgesia occurs so that the patient does not feel faradiza- 
tion, pricking, or even burns. Pain and tenderness are 
frequent — pain in the forehead as if a nail were driven in, 
in the back, in a joint ; tenderness along the spinal column, 
under the breast, and in the inguinal region. Tenderness to 
deep pressure in the left inguinal region has been referred to 
the ovary; such pressure may produce globus and other 
sensations, or even provoke an hysterical fit ; some fits, on 
the other hand, can be cut short by this means. Inguinal 
tenderness may be witnessed even in hysterical men, so that 
its connection with the ovary may well be doubted. 

Reflex actions may undergo modification. The tendon- 
reactions are often exaggerated, both where there is paralysis 
and where there is not ; often there is a sort of attempt at 
ankle-clonus, less commonly a definite ankle-clonus. * But, 
so far as we know, the patellar tendon-reaction is never 
abolished by hysteria. As regards the skin-reflexes, the 
plantar reflex may be in abeyance, or it may take a great 
deal of tickling to obtain it ; and the reflex normally 
obtainable by touching the back of the throat is often absent. 

As to the organic reflexes, retention of urine is common 
enough in hysteria ; involuntary or unconscious passage of 
the urine is far less common, but may yet take place in 
hysterical paraplegia (Buzzard). 

All the special senses of one side may be affected, as we 

* Dr. Gowers, however, considers that a true ankle-clonus is a mark of 
organic disease. 



320 NERVOUS DISEASES. 

have said, in hysterical hemiangesthesia. Further, possible 
affections of the eyes are as follows : photophobia, amaurosis, 
or sometimes color-blindness ; or again concentric narrowing 
of the field of vision ; monocular diplopia ; ophthalmoplegia 
externa possibly in some few cases. Nystagmus is certainly 
uncommon ; if it ever exists in hysteria, its presence suggests 
rather disseminated sclerosis, or multiple neuritis, or tumor ; 
the pupils act normally in hysteria; there is never optic 
neuritis nor atrophy. 

There may be a whole series of abnormalities referable to 
the internal organs ; we will mention the principal of them. 
In hysterical aphonia, a very common and characteristic 
complaint, the patient cannot speak above a whisper, but the 
cough sounds natural, and on application of electricity to 
the larynx the voice will probably return suddenly. Further, 
on inspection the larynx is seen to be structurally normal, 
but there is paresis of the adductors or tensors, allowing a 
chink to remain between the cords, or the cords themselves 
to remain lax during attempts at phonation. Hysterical 
cough is a harsh, monotonous bleat or bark, which may be 
repeated at intervals in the same key for hours together. 
"Globus" is the name applied to the choking feeling or 
lump in the throat, from which most hysterical women suffer 
at times ; it may be associated with curious feelings ascending 
from the lower abdomen, or still more commonly from the 
epigastrium ; or with palpitation of the heart. These often 
form the preludes to an hysterical fit. Dysphagia may reach 
such a degree that it can only be distinguished by the passage 
of a sound from organic disease of the pharynx. Hysterical 
vomiting generally occurs directly after taking food : the 
food returns unchanged, there is no epigastric pain, as in 
gastritis, and despite the apparent rejection of nutriment, the 
patient contrives to maintain her nutrition. Some hysterical 
women are troubled by constant eructations or borborygmi ; 
and sometimes flatulent distention of the abdomen, with 



HYSTERIA. 321 

tenderness, simulating peritonitis, may be witnessed. Reten- 
tion of urine, and the occasional incontinence of urine, we 
have noticed ; a more rare and curious condition has been 
described by Charcot — viz., hysterical suppression of urine. 
In such exceptional cases there is usually vomiting, by which 
means possibly urea may be excreted. We must be careful 
to exclude malingering here. 

Disturbances of nutrition form no part of hysteria as a rule ; 
we will mention two exceptions. First, as to general nutri- 
tion. There is a state, sometimes called "anorexia nervosa," 
in which the patient, a young woman who has usually been 
exposed to some nervous shock or strain, takes a dislike to all 
food, eats less and less, while she vomits apparently what little 
she does take. She emaciates so much that organic disease of 
the stomach or phthsis is feared ; and her sunken, flushed 
cheeks may strongly suggest phthisis. But nothing can be 
found by physical examination ; and her recovery under 
forced feeding, massage, etc., may finally negative such sup- 
positions. Secondly, as to the nutrition of a limb in hysteri- 
cal paralysis. This is usually normal ; but sometimes there is 
considerable wasting. The characteristics of such "hysteri- 
cal atrophy" have been thus stated (Babinski) : it develops 
somewhat rapidly, and when the motor power has returned it 
disappears rapidly \ it may involve the whole limb or seg- 
ments of the limb, but does not pick out particular muscles ; 
there are no fibrillary twitchings ; the muscle contracts nor- 
mally when stimulated by a blow upon its substance ; and the 
electro-contractility is either normal or else quantitatively 
diminished, but there is never reaction of degeneration. 

Treatment. — It is evident not only that the diagnosis 
between hysterical and organic disease is all-important, both 
for purposes of prognosis and of treatment, but also that it 
may often be extremely difficult, and possible only to those 
who have a minute and accurate knowledge of the symptoms 
and course of organic nerve-disease. The treatment of an 



322 NERVOUS DISEASES. 

hysterical patient may be no less difficult ; for it may require 
a more intimate knowledge of her circumstances and disposi- 
tion, and a greater moral authority over her than the physi- 
cian has an opportunity of acquiring. For, unless she enter- 
tain toward him a certain attitude of confidence and submis- 
sion, things will probably not go well. In most severe cases 
it is advisable to remove the patient from the surroundings in 
which the disease has been bred and fostered, and from friends 
whose attentions may be injudicious, or who may have lost 
control over her. She should be placed with some nurse or 
companion whom she can like and respect, and who must be 
firm yet kind and pleasant in her dealings with her. Every 
opportunity must be seized of suggesting* and demonstrating 
to her the fact that she can and will get well. Employment 
and interests should be found for her as soon as she is capable 
of them. And, not least, states of mal-nutrition or of anaemia 
must be rectified, the bowels and catamenia regulated, and 
any real bodily disease or source of irritation treated as effi- 
ciently and quickly as may be. 

The plan of treatment advocated by Weir-Mitchell and 
Playfair is in accordance with these principles. It is most 
useful in cases of hysterical paralysis, and in women who by 
inaction and loss of appetite have become actually weak and 
emaciated. The patient is removed from home and friends, 
and placed in isolation under the charge of a suitable nurse. 
She is confined to bed, and at first her food consists solely 
of three or four ounces of milk every three hours. Then a 
course of massage is gradually begun, and with it the milk is 
increased in amount and solid food given, till within a fort- 
night or so she is taking three full meals daily, besides one or 
two quarts of milk and strong soup. The muscles are usually 
exercised by faradism as well as massage ; and as she regains 

* We do not enter here into the recently revived question of treatment 
by " hypnotic " suggestion. 



TRANCE. 323 

power and nutrition she is encouraged to use her limbs, and 
gradually to pass from invalidism to active habits. Isolation 
from her friends appears to be an essential to this treatment, 
and also the services of a competent nurse, and a masseuse 
who can properly exercise the muscles. Without proper 
massage, tissue change fads, and the overfeeding, the object 
of which is renovation of the tissues, cannot be carried 
on. 

Other modes of treatment are often extremely useful in 
hysteria, as, for instance, shower-baths and cold douches, 
static electricity, faradism to the muscles in cases of paralysis 
or contracture, faradism to the skin by means of the wire- 
brush in cases of anaesthesia. Bromides may be given for fits, 
in small doses, and combined either with tincture of digitalis 
or tincture of valerian. Valerianate of zinc is often useful; 
and, as general tonics, iron, quinine, and nux vomica. Al- 
cohol, opiates, chloral, and similar sedatives, are best avoided. 
We should not be too anxious to treat every symptom as it 
arises ; it may be well to meet some of them with a judicious 
disregard. For instance, retention of urine is apt to be per- 
petuated by the use of the catheter. Hysterical fits may often 
be cut short by one or other of the following methods : — 
Cold water, applied either by slapping her face and neck 
vigorously with a wet towel, or as a profuse and sudden liba- 
tion to her face and head ; or, if this be inadvisable, by pour- 
ing a small stream from a height upon her face, and into her 
mouth if she opens it, her dress and body being protected by 
a towel or mackintosh ; sharp faradism, applied by a wire- 
brush to the skin of the hand or neck ; Hare's method of 
closing the nostrils and mouth with the hand till semistrang- 
ulation is produced ; Charcot's method of so-called ovarian 
pressure. 

Trance. — To the rare conditions of trance and catalepsy 
we shall only just allude. In trance or lethargy (most fre- 
quently seen in hysterical subjects) the patient appears deeply 



324 NERVOUS DISEASES. 

asleep, and cannot be roused ; in extreme cases the respira- 
tions become very shallow and infrequent, and the pulse and 
heart-beat very feeble, and the bodily functions are reduced 
to such a low ebb as more or less to counterfeit death. 

Catalepsy. — Catalepsy is most common in the insane, 
but may be seen sometimes in the hysterical, and a cateleptic 
condition of muscles may occur in the course of various 
organic cerebral diseases. A cataleptic attack generally comes 
on suddenly and under the influence of some powerful emo- 
tion ; the patient appears bereft of consciousness and of the 
power of spontaneous movement, yet muscular contraction is 
so far maintained that the limbs and trunk are immobilised 
in the posture wherein the attack found the patient ; and if 
the limbs be manipulated by a bystander, the postures im- 
printed on them are similarly maintained. Thus the patient 
resembles a living statue which can be moulded to any posi- 
tion. 

Hypnotism. — Similar conditions can be produced by the 
processes known as hypnotism or mesmerism, and not only 
these, but a further condition sometimes called somnambulism. 
In this the patient's mind and body seem to become capable of 
action again; but only of such action as is directed or sug- 
gested by the person who has hypnotised him. He does 
exactly what he is told to do, and appears to adopt any idea 
that is suggested to him. Neither does the influence always 
cease when he is awakened ; commands and suggestions for 
future use, made to him during the hypnotic state, are some- 
times obligatory upon him afterward (post-hypnotic sug- 
gestion). Hypnotism has been largely recommended lately 
for therapeutical purposes, but it would appear to be a double- 
edged weapon. 

Neurasthenia — Neurasthenia is a name now frequently 
applied to a condition which appears to stand midway between 
hysteria and mental disease. The patient, generally a man, 
has few if any objective signs of disease, yet is tormented and 



NEURASTHENIA. 



325 



preoccupied by a series of complaints. In his head he has 
"sensations," a giddiness, a burning, or still more often a 
"pressure" on the vertex, pain at the occiput, tenderness of 
the scalp. He has dimness of vision, spots before the eyes, 
indeed sometimes the visual field, as examined with the 
perimeter, is found to be concentrically narrowed. Tinnitus 
and a certain amount of deafness may be complained of. The 
speech in some cases is indistinct and drawling. 

The spinal region is likewise the seat of aching, weariness, 
pain, or tenderness. In the limbs and trunk there may be 
tinglings, pains, districts of anaesthesia, possibly combined 
with hyper-algesia. The hands may be tremulous, and very 
commonly the legs become feeble, so that the patient walks in 
an uncertain straddling way. Palpitation is common ; loss of 
appetite, loss of sexual desire, and above all sleeplessness or 
bad dreams, are complained of. With all this little is to be 
made out by physical examination, save general feebleness, 
anaesthetic patches possibly, slight exaggeration of tendon- 
reactions ; and, according to Oppenheim, concentric narrow- 
ing of the visual fields ; with optic atrophy and reflex irido- 
plegia in a very few cases. These last two factors, however, 
if present, should raise in our minds a very strong suspicion of 
organic nervous disease, such as spinal degeneration or general 
paralysis. 

The mental condition of these unfortunate people is one of 
depression, of anxiety and alarms, not only about their symp- 
toms, but often of vaguer kinds. They are irritable, unable 
to remember properly, and incapable of applying themselves 
to business. They say they are afraid of committing suicide, 
or of doing injury to others. In some cases attacks of down- 
right insanity have supervened. 

The causes are such as we have had to enumerate for several 
other neuroses — viz., domestic troubles and anxieties, busi- 
ness failures, over application to business-work, perhaps sexual 
excess. The best treatment (which too often cannot be com- 
28 



326 NERVOUS DISEASES. 

passed) is relief from all anxieties, complete and prolonged 
holidays, out-door life in a bracing air with agreeable com- 
panionship. In default of this, tonics and static electricity 
may do something to relieve symptoms. The prognosis 
"quoad vitam" is good, but the "restitutio ad integrum" 
is extremely slow, and often imperfect. The condition may 
be produced by one cause which deserves special mention — 
viz., bodily injury combined with mental shock. The most 
perfect example is a railway accident. The patient has been 
stunned, or at most suddenly alarmed, bruised or shaken ; 
then comes a period of anxiety for his own and others' safety, 
then worry with doctors' examinations and lawyers' cross- 
examinations. The nervous symptoms developing out of all 
these conditions have long received the name of " railway 
spine," but seeing that they may develop after any injury, 
and that the whole nervous centres (not the spinal cord only) 
are affected, the term "traumatic neurosis" has lately been 
proposed. Two cautions must, however, be given : (1) that 
we do not too hastily assume that such symptoms are a pure 
neurosis, for their persistency and some recent pathological 
observations suggest that there may be slight organic changes. 
(2) That when a lawsuit for compensation is impending, the 
possibility of malingering should be carefully and impartially 
weighed. 



MAPS OF MOTOR POINTS. 




rlr. anterior 
acic (pectoralis 
major). 



Ascending frontal and 
parietal convolutions 
(motor area). 

3d frontal convolution 
and insula (centre of 
speech). 

Temporalis. 

Facial {upper branch). 

Facial {trunk). 

Posterior auricular. 

Facial (middle branch). 
Facial [lower bra/uh). 
Splenius. 

Sterno-mastoideus. 
Spinal accessory. 
Levator anguli scapulse. 

Trapezius. 
Dorsalis scapulce 
(rhomboids). 

- Circumflex. 



Long thoracic (serratus) 
magnus). 



§■§ 



-o a c 
"SSft 

ft -rr 3 



Motor Points on Face and Neck. 
(After Erb and De IVatteville.) 



MAPS OF MOTOR POINTS. 
Fig. 62. 



->\ 



329 



Triceps (long head). 



^Deltoid (ante- 
rior portion). 



Musculo- 
cutaneous. 




— Flexor sublimis digitorum. 



Flexor min. digit 
Opponcns min. digit 



Lumbricalcs 



Motor Points on Ufpbr Limii, Flexor Surface. 
(After Erb and DeWaiteville.) 



MAPS OF MOTOR POINTS. 



331 



Fig. 63. 



^ 



Deltoid (pos- — r — ' 
teriorpart). y 



Musculo-spiral. 
Brachialis 



Supinator longus. 
Ext. carpi radial, longior. 
Ext. carpi radial, brevior. 

Extensor communis f 
digitorum. ( 



ndicis. 

Ext. ossis metacarpi 

pollicis. 
Ext. primi internodii 

pollicis. 



Dorsal interossei. \ jj 




Triceps (longhead). 



Triceps (outer head). 



Extensor carpi ulnaris. 
Supinator brevis. 



Extensor minimi digiti. 
Extensor indicis. 



Extensor secundi 
nodii pollicis. 



Abductor minimi digit. 



Dorsal interossei (III & 
IV). 



Motor Points on Upper Limb, Extensor Surface. 
(After Erb and DeWatteviUe.') 



MAPS OF MOTOR POINTS. 



333 



Fig. 64. 



Anterior crural. 



Adductor magnus. 
Adductor longus. 




Vastus internus 



>Tensor fasciae femoris. 

Sartorius. 

Quadriceps femoris. 
Rectus femoris. 

Vastus externus. 



Motor Points on Thigh, Anterior Surface. 
(After Erb and DeWatteville.) 



29 



MAPS OF MOTOR POINTS. 



335 



^ 



Gastrocnemius 
(outer head). 



^r. 1 



iceps (long head). . — , • • jr 

\ ! T 

Do. (short head). _\ 'L M 

\X f 



Adductor magnus. 
j — Semi-tendinosus. 



Flexor longus halluci: 




Posterior tibial. 



Gastrocnemius 
(inner head). 



Flexor longus digitorum. 



Posterior tibial. 



I'oints on Lower Limb, Posterior Surface. 
(After Ei b and />,■ II 'attevtlle. I 



MAPS OF MOTOR POINTS. 



337 



Tibialis amicus 

Extensor longu; 

digitorum. 



Peroneus brevis 



Extensor longus 
hallucis. 



Gastrocnemius. 
Peroneus longus. 




Extensor brevis 
digitorum. 



Abductor minimi 
digiti. 



.Motor Points on Leg, External Surface. 
(After Erb and DeWatteville.) 



NDEX. 



Abscess of brain (vide sub Cerebral 

abscess) 
Agraphia, 119 
Amnesia, 118 

Amyo-trophic lateral sclerosis, 234 
Anaesthesia, 100 
Ankle-clonus, 1 1 3 
Ankle-joint, movements at, 187 
Aphasia, 1 18 
Aphemia, 118 
Aqueduct of Sylvius, 35 
Argyll- Robertson pupil, 132 
Arm, centre for, 61 

depression of, 169 

elevation of, 168 

rotation of, 170 
Arteries of cerebrum, 70 

central, 71 

cortical, 71 
Ataxia, 1 14 

hereditary, 224 

locomotor, 214 
Ataxic paraplegia, 222 
Athetosis, 102 

Atrophy of muscles, arthritic, 244 
Atrophy, progressive muscular, 234, 

243 

Aran-Duchenne type, 237 

Charcot's type, 234 

myopathic type, 23S 

peroneal type, 237 
Auditory centre, 63 
Auditory nerve, 41 

functions of, 143 
Auditory nucleus, 40 
Aura, 292 
Automatism, 293 

Base of brain, 40, 47 
ganglia of, 67 



Bones, disease of, 86 
Brachial plexus, affections of, 181 
Brain (vide sub Cerebrum) 
Broca's convolution, 62 

Cancer of vertebrae, 208 
Capsule, internal, 65-67 

external, 70 
Caries of vertebrse, 206 
Catalepsy, 324 
Centres, motor, of cortex, 60-63 

sensory, 63-64 
Cerebellar disease, symptoms of, 

253 
Cerebellar peduncles, 34 

inferior, 34 

middle, 34 

superior, 34, 50 
Cerebellar tract, 26 
Cerebellum, 51-53 

connections of, 5 1 
Cerebral abscess, 76, 260 

arteries, 70 
Cerebral disease, general symptoms 
of, 250 

localizing symptoms of, 251 

embolism, 85, 267 

hemorrhage, 83, 263 

hemispheres, cortex of, S5~59 

white matter of, 64 

softening, 76, 267 

thrombosis, 86, 254, 267 

tumors, 272 
Cerebro-spinal nerves, 15 

meningitis, 259 
Cerebrum, 55 
Cervical opisthotonos, 259 
Chorda tympani, 42 
Chorea, 101, 241 

hereditary, 303 



339 



340 



Clarke, columns of, 19 
Columns (in spinal cord) 

antero-lateral, 24 

posterior, 27 

posterior vesicular (Clarke's), 

19 
postero- median (Goll's), 28 

postero-lateral (Burdach's), 27 

antero-median (Tiirck's), 25 
(and vide sub Tracts, 
spinal) 
Coma, 1 19 
Conjugate movements, 128 

deviation, 129, 265 
Contracture, 112 
Convulsions, ioi, 251 

epileptiform, 291 

types of, 291 
Corpora quadrigemina, 49 
Cortex cerebri, functions of, 59-64 
Cross-paralysis, 95 
Crura cerebri, 35, 48 
Crusta (or pes pedunculi), 34, 35, 
48 

constituents of, 49 

Decussation of pyramids, 30 

superior, 31 
Defecation, 106 
Degeneration, 77 

ascending, 80 

descending, 80 

diffuse, 82 

primary, 82 

secondary, 78 

systematic, 82 

Wallerian, 78 
Degeneration, reaction of, 155 
Diphtheritic paralysis, 202 
Diplegia, 270 
Diplopia, 125 

Disseminated sclerosis, 225 
Dorsiflexion, 187 
Dura mater, disease of, 86 

spinal, affections of, 206 

cerebral affections of, 254 
Dystrophy, muscular, 240 

Electrical examination, 148 
Epilepsy, 291 



Epilepsy, Jacksonian, 251 
Epileptiform convulsions, 251 
Erb's paralysis, 1S1 
Erect posture, 184 
Eye, fundus of, 132 



Face, centre for, 60 
Facial hemiatrophy, 162 

nerve, 43 

neuralgia, 160 

nucleus, 41 

paralysis, 157 

spasm, 160 
Faradic current, 149 
Fibrae arcuatae, 31 
Fibrillary twitching, 103 
Fifth nerve, deep roots of, 43 

divisions of, 44 

nuclei of, 43, 44 
Fillet, 31, 34, 50 
Fingers, movements of, 1 73 
Fits, causes of, 205 

epileptic, 291 

epileptiform, 291 

hysteroid, 292, 316 

time of, 295 
Fissure of Rolando, 55, 73 

of Sylvius, 56, 74 

parieto-occipital, 56, 76 
Fissures of cerebral cortex, 55, 59 



Foot-drop, 199 
Forearm, movements of, 172 
Fourth nerve, 44 
nucleus, 44 
Friedreich's disease, 224 



Galvanic current, 148 

Ganglia, basic, 67 
functions of, 70 

General paralysis of insane, 230 

Glosso-pharyngeal nerve, 39 
nucleus, 39, 40 
ascending root of, 40 

Hemorrhage, cerebral, 8^, 263 
Headache, "the uric acid," 310 



INDEX. 



341 



Hearing, meatal, 144 

perosseous, 144 

sense of, 143 
Hemicrania, 308 
Hemiparaplegia, 93 
Hemiplegia, 94 

confirmed, 269 

double, 270 

infantile, 271 
Hip-joint, movements of, 185 
Horns of spinal gray matter, ii 

anterior, 18 

posterior, 19 
Hydrocephalus, 279 
Hydromyelia, 247 
Hypnotism, 324 
Hypoglossal nerve, 37 

nucleus, 37 
Hysteria, 313 
Hystero-epilepsy, 316 



Incoordination, 114 
Infantile (spinal) paralysis, 212 
Inflammation of central nervous sys- 
tem, acute, 75 
chronic, 77 
Insular sclerosis, 225 
Inter-olivary layer, 32, 36 
Interossei, paralysis of, 174 
Iridoplegia, reflex, 132 
Iter a tertio ad quartum ventriculum, 
35.49 



JACKSONIAN epilepsy, 25] 



KNEE-JERK, {vide sub Tendon-re- 
action, patellar) 
Knee-joint, movements of, 1S6 



Landry's disease, 210 

Larynx, paralyses of, 163 

Lead-paralysis, 203 

Leg, centre for, 62 

Localization of electrical current, 

'5' 
Lower limbs, muscular mechanism 
of, 1N5 



Lower limbs, muscular nerve-supply 
of, 193 
sensory nerve-supply of, 190 



Medulla oblongata, 30 
Meninges, disease of, 86 
Meningitis, acute, 87 

spinal, 204 

cerebral, 256 

basal, 259 

chronic spinal, 205 

epidemic cerebro-spinal, 259 

syphilitic, 281 

tubercular, 87, 257 
Micturition, 105 
Migraine, 308 
Monoplegia, 96 
Motor paralysis, 91, 97 

points (electrical), 154 

tract, 91 
Muscular atrophy, 233, 243 

arthritic, 244 

dystrophy, 238 
Mydriasis, 131 
Myelitis, acute general, 209 

anterior cornual, acute, 212 

subacute, 213 

cervical, 212 

chronic, 212 

compression, 86, 206 

dorsal, 211 

lumbar, 212 

transverse, 21 1 
Myopathic atrophy, 240 
Myosis, 131 
Myotonia congenita, 242 



Neck, paralysis of muscles of, 183 
Neuralgia, 311 
Neurasthenia, 324 
Neuritis, acute, 196 

peripheral, 197 
Neuroglia, 14 
Nerve-cells, 13 
Nerve-fibres, 13 

medullated, 14 

Qon-medullated, 14 
Nerve-roots, 15 

anterior, [8 



342 



Nerve-roots, posterior, 19 
Nuclei of cranial nerves, 35 
Nucleus ambiguus, 32 

anterolateral of medulla, 32 

auditory, 40 

caudate, 68 

dentate, 52 

facial, 42 

fastigii, 52 

fifth. 43 

fourth, 44 

glosso-pharyngeal, 39, 50 

hypoglossal, 32, 37 

lenticular, 69 

postero- lateral, 31 

postero-median, 30 

post-pyramidal, 31 

red (nucleus tegmenti), 48, 50 

sixth, 42 

spinal accessory, 32, 38 

third, 44 

vagal, 32, 39, 40 
Nystagmus, 126 

Ocular paralysis, 122 

complex, 125 
Olfactory centre, 64 

nerve, 48 

tract, 46 
Olivary bodies, 32, 36 

superior, 42 
Optic atrophy, 135 

nerve, 46 

course of its fibres to brain, 141 

neuritis, 133 

thalamus, 69 

tract, 46 
Otitis, 261 

Pachymeningitis cervicalis, 206 
Palate, paralysis of, 163 
Paresthesia, 102 
Paralysis, acute ascending, 210 

agitans, 304 

choreic, 300 

of ciliary muscle, 131 

diphtheritic, 202 

general, of insane, 230 

motor, 91-94 

lead, 203 



Paralysis, ocular, 122 

pseudo-hypertrophic, 240 

of pupil, 131 

sensory, 98 

of sympathetic, 132 

of third nerve, 1 27 
Paralytic dementia 232 
Paraplegia, 93 

ataxic, 222 

spastic, 221 
Pes pedunculi (vide sub Crusta) 
Petit mal, 294. 
Polar formula, 152 
Polio-myelitis, acute anterior, 212 

subacute anterior, 214 
Pons, region of, 32 
Post- epileptic states, 293 
Posterior longitudinal bundle, 46 

respiratory bundle, 40 
Pott's disease, 206 
Pseudo-hypertrophic paralysis, 240 
Pulvinar, 69 
Pyramids, anterior (of medulla), 30, 

36 
Pyramids, decussation of, 30 

superior, 30 

Qualitative changes (electrical), 

155 

quantitative, 154 

Railway spine, 327 
Reflex actions, 104 

arc, 21, 104, no 
Reflexes, organic, 105 

pupillary, 132 

superficial or skin, 107 

tendon, 108 
Respiration, muscles of, 167 
Restiform bodies, 34 
Reticular formation, 32, 34, 36 
Rigidity of muscle, 112 
Root-symptoms, 207, 245 

Scapula, movements of, 170 

Sciatica, 193 

Sclerosis, 77 

amyo-trophic lateral, 243 
disseminated or insular, 225 
lateral, 221 



343 



Sclerosis, posterior, 214 

postero-lateral (combined), 222 
Sensation, modes of, 98 

paralysis of, 98 
Sensory tract, 92 
Sixth nerve, 42 

nucleus, 42 
Smell, centre for, 64 

sense of, 146 
Spastic paraplegia, 221 
Speech, defects of, 118 
Spinal accessory nerve, 38 

nucleus, 38 
Spinal cord, 16 

cavities in, 247 

diseases, classification of, 209 

functions of, 22 

segments of, iS 

syphilis of, 245 

tumors of, 246 

(and vide sub Myelitis) 
Squint, 124 
Standing, muscular mechanism of, 

184 
Status epilepticus, 295 
Substantia gelatinosa Rolandi, 32 

nigra, 34, 36, 39 
Sylvian aqueduct, 35 

fissure, 55, 74 
Sympathetic nerves, 14 
Syphilis of nervous system, 281 

hereditary, 289 
Syphilitic arteritis, 282 

degeneration, 283 

inflammation, 281 
Syringo-myelia, 247 



Tabes dorsalis, 214 
Taste, centre for, 64 

nerves of, 146 

sense of, 146 
Tegmentum, 34, 36 

constituents of, 49 
Tendon-reactions, 108 
Tendon-reaction, patellar, 108 
Tetany, 303 
Third nerve, 45 

nucleus, 44 
Thomsen's disease, 242 
Thrombosis, cerebral, 85, 255 



Thumb, movements of, 175 
Toes, movements of, 187 
Tongue, paralysis of, 162 
Tract, antero- lateral, 27 

cerebellar, 26 

comma-shaped, 29 

intermedio-lateral, 19 

Lissauer's, 30 

pyramidal, 25 

(and vide sub Columns of cord) 
Tracts, motor, 91 

sensory, 92 

spinal, 24 
Trance, 323 
Tremors, 102 
Trunk, erect position of, 184 

sensory affections of, 182 
Tubercle of Rolando, 14 
Tumors of nervous system, 89 

cerebral, 272 
Tuning-fork, use of, 144 



Upper arm paralysis, 182 
Upper limb, muscular mechanism 
of, 168 

muscular nerve-supply of, 179 

nerves of, 1S0 

sensory nerve-supply of, 178 
Uric acid, 310 



Vagus nerve, 39 

nucleus, 39, 40 
Ventricle, fourth, 33 
Vertebrae, cancer of, 208 

caries of, 206 
Vertigo, 115 

Vessels, disease of 84, 85 
Vesicular columns of Clarke, 19 
Vision, affections of, 138 
Vision, central, 138 

centre for, 64 

color, 142 

field of, 139 



Walking, mechanism of, 189 
Wrist, movement of, 173 
Writer's cramp, 306 
Wryneck, 183 



CATALOGUE No. 7. 



MARCH, 1892. 



A CATALOGUE 

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INCLUDING THE 



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PAGE 
2,3. 



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zette. 

" As it is said of some men, so it might be said of some books, 
that they are ' born to greatness.' This new volume has, we 
believe, a mission, particularly in the hands of the younger 
members of the profession. In these days of prolixity in medical 
literature, it is refreshing to meet with an author who knows both 
what to say and when he has said it. The work of Dr. Goodhart 
(admirably conformed, by Dr. Starr, to meet American require- 
ments) is the nearest approach to clinical teaching without the 
actual presence of clinical material that we have yet seen."— New 
York Medical Record. 

Price of each Book, Cloth, $3.00 : Leather, $3.50. 



THE NEW SERIES OF MANUALS. 



No. 6. PRACTICAL. THERAPEUTICS. 

FOURTH EDITION, WITH AN INDEX OF DISEASES. 

Practical Therapeutics, considered with reference to 
Articles of the Materia Medica. Containing, also, an 
Index of Diseases, with a list of the Medicines 
applicable as Remedies. By Edward John Waring, 
M.D., f.r.c.p. Fourth Edition. Rewritten and Re- 
vised by Dudley W. Buxton, m.d., Asst. to the Prof, 
of Medicine at University College Hospital. 

" We wish a copy could be put in the hands of every Student or 
Practitioner in the country. In our estimation, it is the best book 
of the kind ever written." — N. Y. Medical Journal. 

" Dr. Waring's Therapeutics has long been known as one of the 
most thorough and valuable of medical works. The amount of 
actual intellectual labor it represents is immense. . . . An in- 
dex of diseases, with the remedies appropriate for their treatment, 
closes the volume." — Boston Medical and Surgical Reporter. 

" The plan of this work is an admirable one, and one well calcu- 
lated to meet the wants of busy practitioners. There is a remark- 
able amount of information, accompanied with judicious comments, 
imparted in a concise yet agreeable style." — Medical Record. 

No. 7. MEDICAL JURISPRUDENCE AND 
TOXICOLOGY. 

THIRD REVISED EDITION. 

By John J. Reese, m.d., Professor of Medical Jurispru- 
dence and Toxicology in the University of Pennsyl- 
vania ; President of the Medical Jurisprudence Society 
of Phila. ; Third Edition, Revised and Enlarged. 

*' This admirable text-book." — Amer.Jour. of Med. Sciences. 

" We lay this volume aside, after a careful perusal of its pages, 
with the profound impression that it should be in the hands of every 

doctor and lawyer. It fully meets the wants of all students 

He has succeeded in admirably condensing into a handy volume all 
the essential points." — Cincinnati Lancet and Clinic. 

" The book before us will, we think, be found to answer the ex- 
pectations of the student or practitioner seeking a manual of juris- 
prudence, and the call for a second edition is a flattering testimony 
to the value of the author's present effort. The medical portion 
of this volume seems to be uniformly excellent, leaving little for 
adverse criticism. The information on the subject matter treated 
has been carefully compiled, in accordance with recent knowledge. 
The toxicological portion appears specially excellent. Of that por- 
tion of the work treating of the legal relations of the practitioner 
and medical witness, we can express a generally favorable ver- 
dict." — Physician and Surgeon, Ann Arbor, Mich. 

Price of each Book, Cloth, $3,00; Leather, $3.50. 



6 STUDENTS' TEXT-BOOKS AND MANUALS. 

ANATOMY. 

Macalister's Human Anatomy. 816 Illustrations. A new 
Text-book for Students and Practitioners, Systematic and Topo- 
graphical, including the Embryology, Histology and Morphology 
of Man. With special reference to the requirements of 
Practical Surgery and Medicine. With 816 Illustrations, 
400 of which are original. Octavo. Cloth, 7.50; Leather, 8.50 
Ballou's Veterinary Anatomy and Physiology. Illustrated. 
By Wm. R. Ballon, m.d., Professor of Equine Anatomy at New 
York College of Veterinary Surgeons. 29 graphic Illustrations. 
i2mo. Cloth, 1. 00; Interleaved for notes, 1.25 

Holden's Anatomy. A manual of Dissection of the Human 
Body. Fifth Edition. Enlarged, with Marginal References and 
over 200 Illustrations. Octavo. 

Bound in Oilcloth, for the Dissecting Room, $4.50. 
" No student of Anatomy can take up this book without being 
pleased and instructed. Its Diagrams are original, striking and 
suggestive, giving more at a glance than pages of text description. 
* * * The text matches the illustrations in directness of prac- 
tical application and clearness of detail." — New York Medical 
Record. 

Holden's Human Osteology. Comprising a Description of the 
Bones, with Colored Delineations of the Attachments of the 
Muscles. The General and Microscopical Structure of Bone and 
its Development. With Lithographic Plates and Numerous Illus- 
trations. Seventh Edition. 8vo. Cloth, 6.00 
Holden's Landmarks, Medical and Surgical. 4th ed. Go., 1.25 
Heath's Practical Anatomy. Sixth London Edition. 24 Col- 
ored Plates, and nearly 300 other Illustrations. Cloth, 5.00 
Potter's Compend of Anatomy. Fifth Edition. Enlarged. 
j6 Lithographic Plates. 117 Illustrations. See Page 14. 

Cloth, 1. 00; Interleaved for Notes, 1.25 

CHEMISTRY. 

Bartley's Medical Chemistry. Second Edition. A text-book 
prepared specially for Medical, Pharmaceutical and Dental Stu- 
dents. With 50 Illustrations, Plate of Absorption Spectra and 
Glossary of Chemical Terms. Revised and Enlarged. Cloth, 2.50 

Trimble. Practical and Analytical Chemistry. A Course in 
Chemical Analysis, by Henry Trimble, Prof, of Analytical Chem- 
istry in the Phila. College of Pharmacy. Illustrated. Fourth 
Edition, Enlarged. 8vo. Cloth, 1.50 

4S- See pages 2 to 5 for list of Students' Manuals. 



STUDENTS' TEXT-BOOKS AND MANUALS. 7 

Chemistry : — Continued. 

Bloxam's Chemistry, Inorganic and Organic, with Experiments. 

Seventh Edition. Enlarged and Rewritten. 281 Illustrations. 

Cloth, 4.50; Leather, 5.50 

Richter's Inorganic Chemistry. A text-book for Students. 
Third American, from Fifth German Edition. Translated by 
Prof. Edgar F. Smith, ph.d. 89 Wood Engravings and Colored 
Plate of Spectra. Cloth, 2.00 

Richter's Organic Chemistry, or Chemistry of the Carbon 
Compounds. Illustrated. Second Edition. Cloth, 4.50 

Symonds. Manual of Chemistry, for the special use of Medi- 
cal Students. By Brandreth Symonds, a.m., m.d., Asst. 
Physician Roosevelt Hospital, Out-Patient Department ; Attend- 
ing Physician Northwestern Dispensary, New York. i2mo. 

Cloth, 2.00 

Leffmann's Compend of Chemistry. Inorganic and Organic. 
Including Urinary Analysis. Third Edition. Revised. 

Cloth, 1. 00; Interleaved for Notes, 1.25 

Leffmann and Beam. Progressive Exercises in Practical 
Chemistry. i2mo. Illustrated. Cloth, 1.00 

Muter. Practical and Analytical Chemistry. Fourth Edi- 
tion. Revised, to meet the requirements of American Medical 
Colleges, by Prof. C. C. Hamilton. Illustrated. Cloth, 2.00 

Holland. The Urine, Common Poisons, and Milk Analysis, 
Chemical and Microscopical. For Laboratory Use. Fourth 
Edition, Enlarged. Illustrated. Cloth, 1.00 

Van Niiys. Urine Analysis. Illus. Cloth, 2.00 

Wolff's Applied Medical Chemistry. By Lawrence Wolff, 
M.D., Dem. of Chemistry in Jefferson Medical College. Clo., 1.00 

CHILDREN. 

Goodhart and Starr. The Diseases of Children. Second 
Edition. By J. F. Goodhart, m.d., Physician to the Evelina 
Hospital for Children ; Assistant Physician to Guy's Hospital, 
London. Revised and Edited by Louis Starr, m.d., Clinical 
Professor of Diseases of Children in the Hospital of the Univer- 
sity of Pennsylvania; Physician to the Children's Hospital, 
Philadelphia. Containing many Prescriptions and Formulae, 
conforming to the U. S. Pharmacopoeia, Directions for making 
Artificial Human Milk, for the Artificial Digestion of Milk, etc. 
Illustrated. Cloth, 3.00; Leather, 3.50 

Hatfield. Diseases of Children. By M. P. Hatfield, m.d., 

Professor of Diseases of Children, Chicago Medical College. 

Colored Plate. i:mo, Cloth, 1. 00; Interleaved, 1.25 

$&• See pages 14 and IS /or list of f Quiz-Compends? 



8 STUDENTS* TEXT-BOOKS AND MANUALS. 

Children : — Continued. 
Starr. Diseases of the Digestive Organs in Infancy and 
Childhood. With chapters on the Investigation of Disease, 
and on the General Management of Children. By Louis Starr, 
m.d., Clinical Professor of Diseases of Children in the Univer- 
sity of Pennsylvania. Illus. Second Edition. Cloth, 2.25 

DENTISTRY. 

Fillebrown. Operative Dentistry. 330 Illus. Cloth, 2.50 

Flagg's Plastics and Plastic Filling. 4th Ed. Cloth, 4.00 
Gorgas. Dental Medicine. A Manual of Materia Medica and 
Therapeutics. Fourth Edition. Cloth, 3.50 

Harris. Principles and Practice of Dentistry. Including 
Anatomy, Physiology, Pathology, Therapeutics, Dental Surgery 
and Mechanism. Twelfth Edition. Revised and enlarged by 
Professor Gorgas. 1028 Illustrations. Cloth, 7.00 ; Leather, 8.00 
Richardson's Mechanical Dentistry. Fifth Edition. 569 
Illustrations. 8vo. Cloth, 4.50; Leather, 5.50 

Sewill. Dental Surgery. 200 Illustrations. 3d Ed. CIo., 3.00 
Taft's Operative Dentistry. Dental Students and Practitioners. 
Fourth Edition. 100 Illustrations. Cloth, 4.25 ; Leather, 5.00 
Talbot. Irregularities of the Teeth, and their Treatment. 
Illustrated. 8vo. Second Edition. Cloth, 3.00 

Tomes' Dental Anatomy. Third Ed. 191 Illus. Cloth, 4.00 
Tomes' Dental Surgery. 3d Edition. Revised. 292 Illus. 
772 Pages. Cloth, 5.00 

Warren. Compend of Dental Pathology and Dental Medi- 
cine. Illustrated. Cloth, 1.00; Interleaved, 1.25 

DICTIONARIES. 

Gould's New Medical Dictionary. Containing the Definition 
and Pronunciation of all words in Medicine, with many useful 
Tables etc. % Dark Leather, 3.25; % Mor., Thumb Index 4.25 

Harris' Dictionary of Dentistry. Fifth Edition. Completely 
revised and brought up to date by Prof. Gorgas. 

Cloth, 5.00; Leather, 6.00 

Cleaveland's Pronouncing Pocket Medical Lexicon. 31st 
Edition. Giving correct Pronunciation and Definition. Very 
small pocket size. Cloth, red edges .75 ; pocket-book style, 1.00 

Longley's Pocket Dictionary. The Student's Medical Lexicon, 
giving Definition and Pronunciation of all Terms used in Medi- 
cine, with an Appendix giving Poisons and Their Antidotes, 
Abbreviations used in Prescriptions, Metric Scale of Doses, etc. 
24mo. Cloth, 1. 00; pocket-book style, 1.25 

99- See pages 2 to 5 for list 0/ Students' Manuals, 



STUDENTS' TEXT-BOOKS AND MANUALS. 9 

EYE. 

Hartridge on Refraction. 5th Edition. Illus. Cloth, 2.00 

Hartridge on the Ophthalmoscope. Illustrated. Cloth, 1.50 
Meyer. Diseases of the Eye. A complete Manual for Stu- 
dents and Physicians. 270 Illustrations and two Colored Plates. 
8vo. Cloth, 4.50; Leather, 5.50 

Swanzy. Diseases of the Eye and their Treatment. 158 
Illustrations. Fourth Edition. Cloth, 3 00 

Fox and Gould. Compend of Diseases of the Eye and 
Refraction. 2d Ed. Enlarged. 71 Illus. 39 Formulae. 

Cloth, 1. 00 ; Interleaved for Notes, 1.25 

ELECTRICITY. 

Bigelow. Plain Talks on Medical Electricity and Batteries. 

Illustrated. With a Glossary of Electrical Terms. Cloth, 1.00 
Mason's Compend of Medical and Surgical Electricity. 

With numerous Illustrations. i2mo. Cloth, 1.00 

HYGIENE. 

Parkes* (Ed. A.) Practical Hygiene. Seventh Edition, en- 
larged. Illustrated. 8vo. Cloth, 4.50 

Parkes' (L. C.) Manual of Hygiene and Public Health. 
Second Edition. i2mo. Cloth, 2.50 

Wilson's Handbook of Hygiene and Sanitary Science. 
Seventh Edition. Revised and Illustrated. In Press. 

MATERIA MEDICA AND THERAPEUTICS. 

Potter's Compend of Materia Medica, Therapeutics and 
Prescription 'Writing. Fifth Edition, revised and improved. 
See Page 13. Cloth, 1.00; Interleaved for Notes, 1.25 

Biddle's Materia Medica. Eleventh Edition. By the late 
John B. Biddle, m.d., Prof, of Materia Medica in Jefferson Col- 
lege, Philadelphia. Revised by Clement Biddle, m.d., and 
Henry Morris, m.d. 8vo., illustrated. Cloth, 4.25; Leather, 5.00 

Potter. Handbook of Materia Medica, Pharmacy and 
Therapeutics. Including Action of Medicines, Special Thera- 
peutics, Pharmacology, etc. By Saml. O. L. Potter, m.d., 
m.r.c.p. (Lond.), Professor of the Practice of Medicine in 
Cooper Medical College, San Francisco. Third Revised and 
Enlarged Edition. 8vo. Cloth, 4.00; Leather, 5.00 

Waring. Therapeutics. With an Index of Diseases and 

Remedies. 4th Edition. Revised. Cloth, 3.00; Leather, 3.50 

4W See pages 14 and 15 for list 0/ f Quiz-Compends > 



10 STUDENTS' TEXT-BOOKS AND MANUALS. 

MEDICAL JURISPRUDENCE. 

Reese. A Text-book of Medical Jurisprudence and Toxi- 
cology. By John J. Reese, m.d., Professor of Medical Juris- 
prudence and Toxicology in the Medical Department of the 
University of Pennsylvania ; President of the Medical Juris- 
prudence Society of Philadelphia ; Physician to St. Joseph's 
Hospital ; Corresponding Member of The New York Medico- 
legal Society. Third Edition. Cloth, 3.00; Leather, 3.50 

OBSTETRICS AND GYNAECOLOGY. 

Davis. A Manual of Obstetrics. By Edw. P. Davis, Dem- 
onstrator of Obstetrics, Jefferson Medical College, Philadelphia. 
Colored Plates, and 130 other Illustrations. i2mo. Cloth, 2.00 

Byford. Diseases of Women. The Practice of Medicine and 
Surgery, as applied to the Diseases and Accidents Incident to 
Women. By W. H. Byford, a.m., m.d., Professor of Gynaecology 
in Rush Medical College and of Obstetrics in the Woman's Med- 
ical College, etc., and Henry T. Byford, m.d., Surgeon to the 
Woman's Hospital of Chicago. Fourth Edition. Revised and 
Enlarged. 306 Illustrations, over 100 of which are original. 
Octavo. 832 pages. Cloth, 5.00 ; Leather, 6.00 

Cazeaux and Tarnier's Midwifery. With Appendix, by 
Munde. The Theory and Practice of Obstetrics ; including the 
Diseases of Pregnancy and Parturition, Obstetrical Operations, 
etc. Eighth American, from the Eighth French and First 
Italian Edition. Edited by Robert J. Hess, m.d., Physician to 
the Northern Dispensary, Philadelphia, with an appendix by 
Paul F. Munde, m.d., Professor of Gynaecology at the N. Y. 
Polyclinic. Illustrated by Chromo-Lithographs, and other Full- 
page Plates, seven of which are beautifully colored, and numerous 
Wood Engravings. One Vol., 8vo. Cloth, 5.00; Leather, 6.00 

Lewers' Diseases of Women. A Practical Text-Book. 139 

Illustrations. Second Edition. Cloth, 2.50 

Parvin's Winckel's Diseases of Women. Second Edition. 
Including a Section on Diseases of the Bladder and Urethra. 
150 Illus. Revised. Seepages. Cloth, 3.00; Leather, 3.50 

Morris. Compend of Gynaecology. Illustrated. Cloth, 1.00 

Winckel's Obstetrics. A Text-book on Midwifery, includ- 
ing the Diseases of Childbed. By Dr. F. Winckel, Professor 
of Gynaecology, and Director of the Royal University Clinic for 
Women, in Munich. Authorized Translation, by J. Clifton 
Edgar, m.d., Lecturer on Obstetrics, University Medical Col- 
lege, New York, with nearly 200 handsome illustrations, the 
majority of which are original. 8vo. Cloth, 6.00; Leather, 7.00 

Landis' Compend of Obstetrics. Illustrated. 4th edition, 
enlarged. Cloth, 1. 00; Interleaved for Notes, 1.25 

Galabin's Midwifery. By A. Lewis Galabin, m.d., f.r.c.p. 
227 Illustrations. Seepages. Cloth, 3.00; Leather, 3.50 

4ES~ See pages 2 to 5 for list of New Manuals. 



STUDENTS" TEXT-BOOKS AND MANUALS. 



PATHOLOGY. HISTOLOGY. BIOLOGY. 

Bowlby. Surgical Pathology and Morbid Anatomy, for 
Students. 135 Illustrations. i2mo. Cloth, 2.00 

Davis' Elementary Biology. Illustrated. Cloth, 4.00 

Gilliam's Essentials of Pathology. A Handbook for Students. 
47 Illustrations. i2mo. Cloth, 2.00 

***The object of this book is to unfold to the beginner the funda- 
mentals of pathology in a plain, practical way, and by bringing 
them within easy comprehension to increase his interest in the study 
of the subject. 

Gibbes' Practical Histology and Pathology. Third Edition. 

Enlarged. i2mo. Cloth, 1.75 

Virchow's Post-Mortem Examinations. 3d Ed. Cloth, 1.00 

PHYSICAL DIAGNOSIS. 

Fenwick. Student's Guide to Physical Diagnosis. 7th 
Edition. 117 Illustrations. i2mo. Cloth, 2.25 

Tyson's Student's Handbook of Physical Diagnosis. Illus- 
trated. i2mo. Cloth, 1.25 

PHYSIOLOGY. 

Veo's Physiology. Fifth Edition. The most Popular Stu- 
dents' Book. By Gerald F. Yeo, m.d., f.r.c.s., Professor of 
Physiology in King's College, London. Small Octavo. 758 
pages. 321 carefully printed Illustrations. With a Full 
Glossary and Index. See Page 3. Cloth, 3.00; Leather, 3.50 

Brubaker's Compend of Physiology. Illustrated. Sixth 
Edition. Cloth, 1. 00; Interleaved for Notes, 1.25 

Stirling. Practical Physiology, including Chemical and Ex- 
perimental Physiology. 142 Illustrations. Cloth, 2.25 

Kirke's Physiology. New 12th Ed. Thoroughly Revised and 
Enlarged. 502 Illustrations. Cloth, 4.00 ; Leather, 5.00 

Landois' Human Physiology. Including Histology and Micro- 
scopical Anatomy, and with special reference to Practical Medi- 
cine. Fourth Edition. Translated and Edited by Prof. Stirling. 
845 Illustrations. Cloth, 7.00 ; Leather, 8.00 

" With this Text-book at his command, no student could fail in 

his examination." — Lancet. 

Sanderson's Physiological Laboratory. Being Practical Ex- 
ercises for the Student. 350 Illustrations. 8vo. Cloth, 5.00 

PRACTICE. 

Taylor. Practice of Medicine. A Manual. By Frederick 
Taylor, m.d., Physician to, and Lecturer on Medicine at, Guy's 
Hospital, London ; Physician to Evelina Hospital for Sick Chil- 
dren, and Examiner in Materia Medica and Pharmaceutical 
Chemistry, University of London. Cloth, 4.00; Leather, 5.00 

tfg' See pages 14 and IS for list 0/ t ' Quiz-Compends t 



12 STUDENTS' TEXT-BOOKS AND MANUALS. 

Practice : — Continued. 

Roberts' Practice. New Revised Edition. A Handbook 
of the Theory and Practice of Medicine. By Frederick T. 
Roberts, m.d. ; m.r.c.p., Professor of Clinical Medicine and 
Therapeutics in University College Hospital, London. Seventh 
Edition. Octavo. Cloth, 5.50 ; Sheep, 6.50 

Hughes. Compend of the Practice of Medicine. 4th Edi- 
tion. Two parts, each, Cloth, 1. 00; Interleaved for Notes, 1.25 
Part i. — Continued, Eruptive and Periodical Fevers, Diseases 

of the Stomach, Intestines, Peritoneum, Biliary Passages, Liver, 

Kidneys, etc., and General Diseases, etc. 

Part ii. — Diseases of the Respiratory System, Circulatory 

System and Nervous System ; Diseases of the Blood, etc. 

Physicians' Edition. Fourth Edition. Including a Section 
on Skin Diseases. With Index. 1 vol. Full Morocco, Gilt, 2.50 

From John A. Robinson, M.D., Assistant to Chair 0/ Clinical 
Medicine, now Lecturer on Materia Medica, Rush Medical Col- 
lege, Chicago, 
"Meets with my hearty approbation as a substitute for the 

ordinary note books almost universally used by medical students. 

It is concise, accurate, well arranged and lucid, . . . just the 

thing for students to use while studying physical diagnosis and the 

more practical departments of medicine." 

PRESCRIPTION BOOKS. 

■Wythe's Dose and Symptom Book. Containing the Doses 
and Uses of all the principal Articles of the Materia Medica, etc. 
Seventeenth Edition. Completely Revised and Rewritten. Just 
Ready. 32mo. Cloth, 1. 00; Pocket-book style, 1.25 

Pereira's Physician's Prescription Book. Containing Lists 
of Terms, Phrases, Contractions and Abbreviations used in 



Prescriptions Explanatory Notes, Grammatical Construction of 
Prescriptions, etc., etc. By Professor Jonathan Pereira, m.d. 
Sixteenth Edition. 32mo. Cloth, 1. 00; Pocket-book style, 1.2s 

PHARMACY. 

Stewart's Compend of Pharmacy. Based upon Remington's 
Text-Book of Pharmacy. Third Edition, Revised. With new 
Tables, Index, Etc. Cloth, 1.00; Interleaved for Notes, 1.25 

Robinson. Latin Grammar of Pharmacy and Medicine. 
By H. D. Robinson, ph.d., Professor of Latin Language and 
Literature, University of Kansas, Lawrence. With an Intro- 
duction by L. E. Sayre, ph.g., Professor of Pharmacy in, and 
Dean of, the Dept. of Pharmacy, University of Kansas. i2mo. 

Cloth, 2.00 

SKIN DISEASES. 

Anderson, (McCall) Skin Diseases. A complete Text-Book, 

with Colored Plates and numerous Wood Engravings. 8vo. 

Cloth, 4.50; Leather, 5.50 

Van Harlingen on Skin Diseases. A Handbook of the Dis- 
eases of the Skin, their Diagnosis and Treatment (arranged alpha- 
betically). By Arthur Van Harlingen, m.d.. Clinical Lecturer 
on Dermatology, Jefferson Medical College; Prof, of Diseases of 
the Skin in the Philadelphia Polyclinic. 2d Edition. Enlarged. 
With colored and other plates and illustrations. i2mo. Cloth, 2.50 
■*^» See pages 2 to 5 for list of New Manuals. 



STUDENTS' TEXT-BOOKS AND MANUALS. 13 
SURGERY AND BANDAGING. 

Moullin's Surgery, A new Text-Book. 500 Illustrations (some 
colored), 200 of which are original. 

Cloth, net 7.00; Leather, net 8.00 

Jacobson. Operations in Surgery. A Systematic Handbook 
for Physicians, Students and Hospital Surgeons. By W. H. A. 
Jacobson, B.A., Oxon. f.r.c.s. Eng. ; Ass't Surgeon Guy's Hos- 
pital ; Surgeon at Royal Hospital for Children and Women, etc. 
199 Illustrations. 1006 pages. 8vo. Cloth. 5.00; Leather, 6.00 

Heath's Minor Surgery, and Bandaging. Ninth Edition. 142 
Illustrations. 60 Formulae and Diet Lists. Cloth, 2.00 

Horwitz's Compend of Surgery, .Minor Surgery and 
Bandaging, Amputations, Fractures, Dislocations, Surgical 
Diseases, and the Latest Antiseptic Rules, etc., with Differential 
Diagnosis and Treatment. By Orville Hokwitz, b.s., m.d. s 
Demonstrator of Surgery, Jefferson Medical College. 4th edition. 
Enlarged and Rearranged. 136 Illustrations and 84 Formulae. 
i2mo. Cloth, 1.00 ; Interleaved for the addition of Notes, 1.25 
***The new Section on Bandaging and Surgical Dressings, con- 
sists of 32 Pages and 41 Illustrations. Every Bandage of any 
importance is figured. This, with the Section on Ligation of 
Arteries, forms an ample Text-book for the Surgical Laboratory. 

Walsham. Manual of Practical Surgery. Third Edition. 
By Wm. J. Walsham, m.d., f.r.c.s., Asst. Surg, to, and Dem 
of Practical Surg, in, St. Bartholomew's Hospital; Surgeon to 
Metropolitan Free Hospital, London. With 318 Engravings. 
See Page 2. Cloth, 3.00; Leather, 3.50 

URINE, URINARY ORGANS, ETC. 

Holland. The Urine, and Common Poisons and The 
Milk. Chemical and Microscopical, for Laboratory Use. Illus- 
trated. Fourth Edition. i2mo. Interleaved. Cloth, 1.00 

Ralfe. Kidney Diseases and Urinary Derangements. 42 Illus- 
trations. i2mo. 572 pages. Cloth, 2. 75 

Marshall and Smith. On the Urine. The Chemical Analysis of 
the Urine. By John Marshall, m.d., Chemical Laboratory, Univ. 
of Penna ; and Prof. E. F. Smith, ph.d. Col. Plates. Cloth, 1.00 

Tyson. On the Urine. A Practical Guide to the Examination 
of Urine. With Colored Plates and Wood Engravings. 7th Ed. 
Enlarged. i2mo. Cloth, 1.50 

Van Niiys, Urine Analysis. Illus. Cloth, 2.00 

VENEREAL DISEASES. 

Hill and Cooper. Student's Manual of Venereal Diseases, 
with Formulae. Fourth Edition, umo. Cloth, 1.00 

Jt&~ See pages 14 and 15 for list 0/ f Quiz-Compends ? 



NEW AND REVISED EDITIONS. 

PQUIZ-COMPENDS? 

The Best Compends for Students' Use 
in the Quiz Class, and when Pre- 
paring for Examinations. 

Compiled in accordance with the latest teachings of promi- 
nent lecturers and the most popular Text- books. 

They form a most complete, practical and exhaustive 
set of manuals, containing information nowhere else col- 
lected in such a condensed, practical shape. Thoroughly 
up to the times in every respect, containing many new 
prescriptions and formulae, and over two hundred and 
fifty illustrations, many of which have been drawn and 
engraved specially for this series. The authors have had 
large experience as quiz-masters and attaches of colleges, 
with exceptional opportunities for noting the most recent 
advances and methods. 

Cloth, each $1.00. Interleaved for Notes, $1.25. 
No. 1. HUMAN ANATOMY, "Based upon Gray." Fifth 
Enlarged Edition, including Visceral Anatomy, formerly 
published separately. 16 Lithograph Plates, New 
Tables and 117 other Illustrations. By Samuel O. L. 
Potter, m.a., m.d., m.r.c.p. (Lond.,) late A. A. Surgeon U. S. 
Army. Professor of Practice, Cooper Medical College, San Fran- 
cisco. 
Nos. 2 and 3. PRACTICE OF MEDICINE. Fourth Edi- 
tion. By Daniel E. Hughes, m.l>., Demonstrator of Clinical 
Medicine in Jefferson Medical College, Philadelphia. In two parts. 
Part I. — Continued, Eruptive and Periodical Fevers, Diseases 
of the Stomach, Intestines, Peritoneum, Biliary Passages, Liver, 
Kidneys, etc. (including Tests for Urine), General Diseases, etc. 

Part II. — Diseases of the Respiratory System (including Phy- 
sical Diagnosis), Circulatory System and Nervous System; Dis- 
eases of the Blood, etc. 

*** These little books can be regarded as a full set of notes upon 
the Practice of Medicine, containing the Synonyms, Definitions, 
Causes, Symptoms, Prognosis, Diagnosis, Treatment, etc., of each 
disease, and including a number of prescriptions hitherto unpub- 
lished. 

No. 4. PHYSIOLOGY, including Embryology. Sixth 
Edition. By Albert P. Brubaker, m.d., Prof, of Physiology, 
Penn'a College of Dental Surgery ; Demonstrator of Physiology 
in Jefferson Medical College, Philadelphia. Revised, Enlarged, 
with new Illustrations. 
No. 5. OBSTETRICS. Illustrated. Fourth Edition. By 
Henry G. Landis, m.d., Prof, of Obstetrics and Diseases of 
Women, in Starling Medical College, Columbus, O. Revised 
Edition. New Illustrations. 



BLAKISTON'S ? QUIZ-COMPENDS ? 

No. 6. MATERIA MEDICA, THERAPEUTICS AND 
PRESCRIPTION WRITING. Fifth Revised Edition. 
With especial Reference to the Physiological Action of Drugs, 
and a complete article on Prescription Writing. Based on the 
Last Revision of the U. S. Pharmacopoeia, and including many 
unofficinal remedies. By Samuel O. L. Potter, m.a., m.d., 
m.r.c.p. (Lond.,) late A. A. Surg. U. S. Army; Prof, of Practice, 
Cooper Medical College, San Francisco. Improved and Enlarged, 
with Index. 

No. 7. GYNAECOLOGY. A Compend of Diseases of Women. 
By Henry Morris, m.d., Demonstrator of Obstetrics, Jefferson 
Medical College, Philadelphia. 45 Illustrations. 

No. 8. DISEASES OF THE EYE AND REFRACTION, 
including Treatment and Surgery. By L. Webster Fox, m.d., 
Chief Clinical Assistant Ophthalmological Dept., Jefferson Med- 
ical College, etc., and Geo. M. Gould, m.d. 71 Illustrations, 39 
Formulas. Second Enlarged and Improved Edition. Index. 

No. 9. SURGERY, Minor Surgery and Bandaging. Illus- 
trated. Fourth Edition. Including Fractures, Wounds, 
Dislocations, Sprains, Amputations and other operations ; Inflam- 
mation, Suppuration, Ulcers, Syphilis, Tumors, Shock, etc. 
Diseases of the Spine, Ear, Bladder, Testicles, Anus, and 
other Surgical Diseases. By Orville Horwitz, a.m., m.d., 
Demonstrator of Surgery, Jefferson Medical College. Revised 
and Enlarged. 84 Formulae and 136 Illustrations. 

No. 10. CHEMISTRY. Inorganic and Organic. For Medical 
and Dental Students. Including Urinary Analysis and Medical 
Chemistry. By Henry Leffmann, m.d., Prof, of Chemistry in 
Penn'a College of Dental Surgery, Phila. Third Edition, Revised 
and Rewritten, with Index. 

No. 11. PHARMACY. Based upon " Remington's Text-book 
of Pharmacy." By F. E. Stewart, m.d., ph.g., Quiz-Master 
at Philadelphia College of Pharmacy. Third Edition, Revised. 

No. 12. VETERINARY ANATOMY AND PHYSIOL- 
OGY. 29 Illustrations. By W11. R. Ballou, m.d., Prof, of 
Equine Anatomy at N. Y. College of Veterinary Surgeons. 

No. 13. DENTAL PATHOLOGY AND DENTAL MEDI- 
CINE. Containing all the most noteworthy points of interest 
to the Dental student. By Geo. W. Warren, d.d.s., Clinical 
Chief, Penn'a College of Dental Surgery, Philadelphia. Illus. 

No. 14. DISEASES OF CHILDREN. By Dr. Marcus P. 
Hatfield, Prof, of Diseases of Children, Chicago Medical 
College. Colored Plate. 

Bound in Cloth, $1. Interleaved, for the Addition of Notes, $1.25. 

jgggf* These books are constantly revised to keep up with 
the latest teachings and discoveries, so that they contain 
all the new methods and principles. No series of books 
are so complete in detail, concise in language, or so well 
printed and bound. Each one forms a complete set of 
notes upon the subject under consideration. 

Illustrated Descriptive Circular Free. 



JUST PUBLISHED. 



GOULD'S NEW 

Medical Dictionary 




PRAGTIGAL. 



COMPREHENSIVE 



It contains Tables of the Arteries, Bacilli, Gan- 
glia, Leucomaines, Micrococci, Muscles, 
Nerves, Plexuses, Ptomaines, etc., 
etc., that will be found of great 
use to the student. 



Small octavo, 520 pages, Half-Dark Leather, . #3.25 
With Thumb Index, Half Morocco, marbled edges, 4.25 



From J. M. DaCOSTA, M. D., Professor of Practice and 
Clinical Medicine, Jefferson Medical College, Philadelphia. 

"I find it an excellent work, doing credit to the learning and 
discrimination 0/ the author." 

*** Sample Pages free. 



